You can tell when someone REALLY knows their stuff - they are able to explain it so even nonprofessionals can understand the main points. They tread the fine line between glossing over and going too deep. Dr. Campbell really explained this all so well. Not saying I'll retain it all - but I have a much better understanding than I did before.
🎯 Key Takeaways for quick navigation: 00:00 🛡️ Cholesterol alone is not a strong predictor of heart disease events; it's the particle number that matters. 02:17 🎾 Cholesterol is transported in the blood via lipoprotein particles, like LDL and HDL. 06:17 🔄 LDL cholesterol and LDL particle count can disagree; risk is linked to particle count, not cholesterol levels. 10:11 💼 Discordance between cholesterol and particle number is common, especially in conditions like diabetes. 13:23 📊 LDL particle number, not cholesterol, significantly predicts heart disease events, especially with therapy. 16:32 🚀 Guidelines often aim for general population health; individual cases may require more nuanced assessments. 19:45 📋 Understanding individual risk factors, including LDL particle count, is crucial for personalized heart health. 22:41 🔍 Inflammation becomes more significant in advanced atherosclerosis, but it's not the primary initiator of plaque formation. 23:29 🩺 Chronic inflammatory conditions, like psoriatic arthritis, are associated with plaque formation due to arterial damage. 24:21 🩸 ApoB-containing lipoproteins, which contribute to plaque formation, move into the artery wall through a process called transcytosis. 25:31 🔧 The "response to retention" model suggests that once lipoproteins enter the artery wall, they need additional modifications to initiate plaque formation. 26:52 🚫 Triglyceride Rich Remnant particles are more atherogenic and contribute more quickly to plaque formation compared to LDL particles. 27:46 🧬 Type 3 Dyslipoproteinemia leads to the accumulation of atherogenic particles, causing rapid plaque formation. 29:03 🌊 Lowering LDL levels doesn't necessarily reduce all ApoB particles, and elevated triglyceride Rich remnants can still lead to heart events. 30:20 🩸 Modulating transcytosis or post-retention oxidation specifically is not currently possible. The primary focus should be on overall physiological health. 33:10 🛡️ Foam cell formation is the critical step in atherosclerosis. Reducing atherogenic particles helps prevent plaque formation. 35:03 📊 The risk of plaque formation depends on the concentration of lipoproteins that enter the artery wall, influenced by various factors like endothelial damage and lipoprotein levels. 38:04 🌱 Lifestyle changes, like managing blood pressure, glucose levels, cholesterol, and insulin resistance, are crucial for reducing plaque formation. More specific interventions are still under research.
Incredible! Thank you for summarizing so extremely well. This channel combined with good people like you literally make this a college level course on survival. Seriously, putting these pieces together over time is a roadmap for long life and healthy living. 👍👍👍
After having read this summary & relating this current information to decades past information, a lot needs to be changed because they are already proven wrong.
Everyone should listen to this presentation. At least if not everyone, all cardiologists and primary care physicians should watch this. Incredibly informative and easy to understand. I sincerely hope that Dr. Cromwell will get invited back for a few more episodes.
When I was going through chemo, and having regular CT Scans, they found two blockages. I talked to my Radiation Oncologist about it, and he said 'Not to worry'. I wish he had said 'Game on'. Maybe I would not have had the massive heart attack - maybe I would have changed my diet. I will admit to getting quite lost, watching this, but I will watch it a few more times, and pick up a bit more each time.
What a great video. Often times we lose the nuance in medicine but Dr. Cromwell does a great job of explaining it. This needs to be required viewing for anyone who wants to take control of their own health.
38:22 Layman's explanation: Eat whole, non-processed foods instead of ultra-processed foods however and whenever possible. Don't overeat. Be active. Pass around five forks for one dessert. Don't smoke. Don't drink alcohol unless you can stop at one drink. Recent data is suggesting to just quit. That should be it.
Fantastic interview. Thank you! You are doing a phenomenal job educating the public. Had a couple of questions. 1. Is it only LDL particles stuck in the intima that can be damaged or can freely flowing LDL particles be damaged if exposed to glucose/insulin in the bloodstream. 2. Are all damaged LDL particles stuck in the arterial wall or can they come loose and get back into the bloodstream. 3. If damaged particles can get back in the bloodstream, can the LDL receptors on the liver still pick them up. 4. How do you balance the risks of lowering LDL particles with a statin versus the side effect of the statin (which may include causing diabetes), especially in the population that is low risk of getting plaque buildup even with a high apo-b count. 5. Does the triglyceride count and /or the insulin resistance increase risk of starting plaque formation (not increasing existing plaque formation which he said was almost certain).
@@paulgaras2606 Wow. YT just deleted my response comment and gave me a big personal warning about it. I explained how to get around the problems you have with the YT app. They're just plain mean and sore losers. I guess I can only tell you there are ways around it....
@@paulgaras2606 No you don't. You simply play the video on your phone and listen to it on earphones or via the phone's speaker. I just did that very thing and it works fine (other than having to skip through the ads).
The information you provide on your channel helped me understand that I needed to reduce saturated fats, which brought my LDLc down by 25%. Thank you! Can't wait to see my Dr. in a couple days! Now as long as I'm not one of the ones where that's an inaccurate measure ....
Thank you Mr. Cromwell. The approach you take to the subject of Cardiovascular problems is scientifically honest without fanaticism, comprehensive and without placing yourself on any side of the conflicting parties
why don't we make things easy for everyone- just measure APOB as it tracks cause/risk better? not sure why we are still having this discussion. apoB test is like 30 bucks. why not run both?
Trying not to wear my tin foil, it's likely that there is just too much money to be made doing it the way they've been doing it all these years. I wholeheartedly agree with you though. Thanks to Dr. G, I learned that ApoB is a thing and had mine tested. It's extremely high, and diet and exercise has changed!!!!
@@billusingh3439Every person responds differently. I only need 30mg Rosuvastatin to lower APOB from 129 to 59. Someone else may need multiple drugs, including expensive PCSK9 inhibitors, to achieve that. Talk to your doctor and experiment together.
Wow! The best video on the subject I've seen/heard. Please put the auto-translate in all languages captioning on for my non-english speakers like my wife who thinks all is fine. Thanks, dr. Carvalho & Cromwell.
Such a fantastic channel and interview. Second time I watched this. Dr. Cromwell is so lucid, you can't help but understand, and Dr. Carvalho's summary at the end helps to get you to the practical application of what you learned to protect your cardiovadcular health.
Just brought my wife home from the hospital after having a 95% blockage in one and 80-90% in another. Amazingly good cholesterol levels. Unfortunately, it is probably genetic and does tend to run in her family. But I agree, just the cholesterol numbers are not a very good predictor of heart disease. Total cholesterol was 147 and LDL was 72. Believe it or not they were going to put her on a statin. So far they haven't.
I'm working my way through this very helpful video. I recently had blood work done in preparation for my annual physical, and asked if the could add an APoB test, thanks to Dr. Gil's videos. What I didn't know until after I'd had the blood drawn is that it takes a good week to get the APoB results back from the lab, instead of the normal 24-48-hour turnaround.
Great video. After I finish it I will check your other videos about it and saturated fat that I watched but didn't grasped fully. Good explanations. I think now I got it more fully.
The lifestyle measures of heart disease risk: 1) Are you overweight? (BMI above 25): No. 2) Do you get angry when I ask what your waist measurement is? No. 3) Do you smoke at all? No. 4) Do you drink more than very occasionally? No. 5) Do you eat a plant *biased* diet with the majority of your calories coming from whole (high fibre) foods? Very low in saturated fats. Yes 6) Do you exercise; about 5 hours a week *brisk* walking with hills and stairs or equivalent plus some weight/isometrics? Yes. That covers all the practical things you mention in your other videos. My theory is most people who are obsessed with biomarkers are trying to find a reason those questions don't apply to them!
I don't know about most people but I don't fit the normal model of a high risk person (no family history of early events, never smoked, BMI of 22 and regular exercise for many decades, no symptoms, etc.) so when I got a "severe" coronary artery calcium scan, biomarkers became the way to measure my progress in reducing risk. Hopefully that's what other people who're smart enough to watch this video are doing with them also.
In my original point I say *most* people are trying to get out of one of the items on the list and you haven't said you have done all the things in the list - plus you might not be *most* people.
I've decided that every expert has valid points. Every meta study has valid assertions. Every individual has to realize that neither of those two facts mean much to their particular health condition. It is a roll of the dice because of too many unknown factors in our bodies.
- Dr William Cromwell is a clinical lipidologist, professor at Wake Forest University School of Medicine, and he has published many studies on lipid physiology and metabolic disease. 10:05 chapter on the discordance between LDL-C and ApoB: he said that 30-50% of healthy people have such discordance, while metabolically unhealthy people are more likely to have discordance (up to 70% of them have it). he also says there is no discordance when LDL-C is very high or very low.
Sad to hear this info cant go mainstream because the old view of cholesterol is too deeply lodged into our healthsystem. Thanks for these type of videos, greatly appreciated to get information from suxh a knowledgable person
Despite eating a plant based diet and exercising frequently I discovered through advanced screening that my risk for diabetes and heart disease is higher than I expected and much higher than I want. I am currently using fiber supplementation and sodium reduction to reduce my risk and then I am going to re-test. I already noticed that my blood pressure has come down since I started the interventions. I'm very excited to see how well these interventions have worked to reduce my risk but I'm trying to wait because the testing is fairly expensive and I want to give it time to work.
Try switching to a WFPB (if you don't practice it already) and try using very little salt, or using combinations of sodium-free salt and sodium-containing salt. You can find more information about this on Gil's video on the best salt for health, where he discusses a sodium-free version of salt. Read the comment section on the video too, people there had good suggestions.
Good work on adapting! I had to do the same thing, even though I was eating a whole food plant based diet like you, I ended up having to exercise more, get rid of ground grains from my diet (bread, pasta, etc), potatoes, and salt. I also added some potassium chloride. With these changes, over the course of a few months my numbers moved into optimal range.
@@Teneab thanks I already try to eat WFPB for the most part but the junk creeps in. Part of the intervention is trying to avoid the plant based junk as well. I’ve been using a 50/50 blend of potassium chloride and salt and using less of that overall. I have lost weight and I feel like I’m really on the right track. Wishing you good health!
@@bgrune1 Oh sounds like you are already doing everything correctly, lol! Keep up the great work. Have you checked your ApoB or cholesterol since you've started the intervention?
Hello Doc: can you share your diet and lifestyle (sleep, exercise, anything else important) for good health? Since you have researched a variety of topics over the years, I imagine you follow some best practices. Thank you so much
While this is an interesting conversation, I'm not sure how useful it will be to the average viewer. I appreciate the technical explanation of why measuring cholesterol isn't perfectly accurate to every individual, but I don't know how to apply this information to a real-life scenario. Basic information on how to manage the potential risk factors (like exercise, smoking cessation, drinking cessation, lowering cholesterol, etc.) would be more practical for me. In what way does the information presented here change the advice given to the general public? If someone were to ask me what causes heart disease, I wouldn't know how to translate this information in a way for them to practically understand.
good question. the general knowledge to heed high glucose, blood pressure or cholesterol levels is directionally correct but can miss risk factors in many people, hence knowing insulin resistance metrics, ApoB or nonHDL-cholesterol can provide more information. also see some of our previous content on heart disease where we touch on a lot of the basics like diet tips, lipid panel etc. In response to that, many viewers asked for more detailed videos on the mechanistic & molecular aspects and that's what this series partly aims to cover
Thanks, that helped to clarify a lot of the misunderstandings I was having. So this is just more accurate information that we can use to in order to assess hidden risk factors.
Where has he been? Love the info, but what about specific numbers of what is too high, target numbers? what about any of the usual ratios? & What about HDL, Triglycerides, & ApoA?
Dr. Cromwell is a great doctor. However, it would be great if Dr. Cromwell would continue to treat his patients that are dependent upon him to answer questions and fill prescriptions.
Great episode Gil! My insight about this metabolic problem with the foam cells etc is that some prolonged fasting could be an amazing method to prevent issues.
But will your insurance pay for the scan? I received a scan from my cardiologist who found nothing after an odd EKG and strong echo; 6 weeks later I had my heart attack and got 4 stents. The term 'worthless" comes to mind.
Thanks so much for the video. I've been plant-based for 11 years now and have listened to Drs Esselstyn and Greger to get my LDL below 75 and total cholesterol to below 150. So now I need to make sure my apoB is below 100 mg/dL? Thanks Gil!!!
I'm from a family w catastrophic heart attacks, high blood pressure, and very high cholesterol which IS added to by diet. I however have very high cholesterol (yhe highest was almost 400 LDL). On pravastatin as it doesn't cause brain issues or joint and muscle pain. Down to almost satisfactory levels by medical standards, but too low (ideal level) is brain foggy and memory issues. No calcium in heart also. I'm about finished with worrying about my cholesterol and trying to get it lower. No heart issues at this time, and those who had catastrophic heart attacks or issues were already showing problems before they died
I flat out told my doctor that I wanted him to order an ApoB test and his response..."We don't do that unless there is a problem.' Like what?!? He can order whatever tests he wants for me and why does he care what test that I want done? I am paying for it and all it does is give him more information. Because I asked for it he won't do it? Ok, so what if a lipid panel came back with numbers that he didn't want to see and then he calls me back in to get the ApoB that I asked for? That is literally a couple hours of time on my part, another blood draw, etc. If I was working, that would be more time that one would have to take off of work. Very inconsiderate at the minimum. What doctor would care if you ask for some benign test that simply uses some of the blood that they are already drawing from you?
great video - amazingly educational. questions: is there a way to reduce plaque if it is formed and can grow? habitual, dietary not intervention ways. similarly = what we can do to lower APO-B?
Hi Gil. I love your videos and subscribe to your channel. Thanks. I would really like to hear your opinion about the new abstract from March 18, 2024 from the American Heart Association: "8-hour time-restricted eating linked to a 91% higher risk of cardiovascular death". It's hard to know what's right and what's not these days.
Hey, can you please consider making a video on Chonline, the possible deficiency of it in lacto-vegetarians and vegans and how those two groups can have sufficient levels? PS: Again, posted this on twitter too but again I have doubts twitter is working properly or may be censoring tweets for some reason.
Fantastic video! Dr. Cromwell says at 25:30 that "once you're in" it's not guaranteed that you'll "stir the pot and cause problems." Does this mean that oxidization has some specific cause? Or is it entirely that certain types of particles get oxidized and others don't? Asked another way - is it the particle type that determines retention + oxidization, or are there other mechanisms that cause more retention and oxidization?
You cannot prevent arrhythmia with a pacemaker. A pacemaker just lowers hb per min. Some people have episodes of afib...but when not in afib their hb is very low already. That is why ablation is the no 1 procedure for afib...but it doesn't always work.
What about the importance of keeping the functionality of HDL to improve cholesterol efflux? How can the fonctionality of HDL be increased? Also I would have liked to know if lowering LDL a lot doesn't lead to problems in other tissues? Some say that going as low as possible is ok, is it true? It seems for instance than in old age people need more LDL.
I'd also like an explanation as to why LDLs only cross the endothelium at a single site (the plaque site) rather than spreading out along every centimetre of artery wall. After 4 million years of evolution, you'd have thought that we would mitigate the problem of atherosclerosis by spreading out the problem over the entire blood system rather than focussing in on a few discrete spots until they become inflamed and rupture. It can't be a coincidence that plaques more ofter occur at branches and confluences in the arteries, more prone to damage caused by eddy currents, high pressure and abrasives.
What should patients do? I’m trying to get my brother to the doctor. He has a huge gut, fat face, and we have diabetes in both sides of our family. Do doctors get upset if you come in and ask for tests? My numbers are ok, says my doctor, but I know I have a problem too because my blood sugar goes up when I eat certain foods. Thanks Docs, both of you, for sharing your knowledge.
The way I look at it is with this formula: (Non-HDL-C / Amount of atherogenic particles) = average particle size. Since ApoB measures the number of atherogenic particles, let's separate it in the formula, and we get: ApoB = (Non-HDL-C / average particle size). So, to optimize ApoB, we should try to optimize two things: 1. Reduce Non-HDL-C 2. Increase particle size Looking at Non-HDL-C is just half of the equation. So, my question is: As lab tests can already measure Non-HDL-C, and most people don't have access to ApoB measurements, how can we estimate the average particle size by other results and determine if Non-HDL-C is an accurate representation of our risk?
As long as you can count the number of particles, the particle size is not predictive of ASCVD events. The misnomer of "small dense & "big fluffy" boils down to: "where there are a lot of them (particles) crammed into the same space (unit of blood), then they are more dense (smaller)." Getting insulin sensitive AND reducing particle number is the name of the game.
@mattbmartin Seems like you did not understand clearly what I wrote. The average particle size does matter but not as a single measurement. It should be combined with Non-HDL cholesterol since together they can predict ApoB
@@lotembenatar7163 Particle size is not relevant to risk because all atherogenic lipoprotein particles are small enough to get into the arterial wall.
Dr . I take Burlinta and I have one stent in my arteries . But I work out daily and eat very healthy can I stop taking Burlinta . I feel strong and healthy now
36:42 When contradictory knowledge and findings are accepted as valid, then we may have to think of a new model to accommodate these different results. This reminds me of a similar dilemma in the world of Physics, and how I learned in physics class that light can be described both as a wave or as discrete particles. I was told that someday a new model might be developed that accommodates both theories of what light really is. But I digress.
Can someone explain to me something, please: I understand the notion of measuring cholesterol versus particle count, especially the ApoB marker for seeing how many lipoprotein transporters there are. I understand that these transports can be packed full of cholesterol/triglycerides, but what triggers the creation of lipoprotein carriers themselves? Does the body make more to respond to excess cholesterol/triglycerides in the blood?
Yes; no excess cholesterol/triglycerides(i.e. fats), no need for the body to make ApoB. ApoB is there just to wrap around cholesterol/triglycerides and help them dissolve into the blood (which is mostly water), since they (fats) are unable to do so by themselves.
This might be a stupid question. But can you please explain (in a scenario where APO-B is high and LDL is low) how that leads to cardiovascular disease? To explain my question, I will use this analogy. Let's say I have 10 people with bad intentions that want to get from point A to B to cause harm. And, there are 100 cars available to transport them with each car able to transfer one person. Once all ten have been transported, the remaining 90 cars on their own can't cause any harm as there are no more ill intentioned passengers to transport. They are empty. But not for the cars, there would be no harm done at point B. But, if there are more cars than bad intentioned people, how do the cars cause more harm? Thanks for the great video. It would just be great to have a better understanding of the actual numbers of APO-B vs LDL in a situation where LDL is low and APO-B is high. Thanks again!!!
It´s rarely discussed one of the most important metrics of health, possibly the most. The omega 3 to omega 6 ratio in your tissues, ideally 1:1 and even 1:3 is within healthy range. Balance is key. If your omega 3 is low you´ll have to tightly handle your omega 6 s. If your omega 6 s are through the roof you´ll have to push your omega 3 through the roof. Some believe that omega 3 s are magic pills that will make all your body problems evaporate. They are not, but still very helpful.
I enjoy these interviews with lipidologists. Because of the last few I've seen, I have gone back on a statin. I have low bmi, zero calcium cacs.....etc etc. My remnant cholesterol is extremely low, but after learning that the number of particles is a driving factor, I decided to make this change. It would be good to see a video explaining apo b and ldl particles. Is apo b the size of the ldl particles? If that's the case, mine are the fluffy A ones based upon all other information.
ApoB is the mass (remember mass is independent of the force of gravity so your mass is the same on Earth and the Moon) of the ApoB containing particles in a deciliter of blood. The units of measure are mg/dl. It is my understanding that LDL particle number is a numerical count of LDL particles. The units of measure are nanomoles per liter of blood. One mole is 6.022 times 10 to the 23rd power. A nanomole is one billionth of that.
is there a rate of clearance of atherosclerosis? in other words, is our body able to clear a little bit of atherosclerosis over time, if health parameters are optimal? in other words, is atherosclerosis in a constant dynamic equilibrium between clearance and accumulation?
Google what happened in Norway in 1940, mortality from circulatory diseases. When Germans occupied Norway, they sent all meats and dairy products to the eastern front, in effect turning Norway vegan. It resulted in a nearly instantaneous 20% drop in cardiac/stroke mortality. The coroners saw these shadowed areas in the arteries of deceased Norwegians that were, they think, where plaques once were present. It would appear if you calorie restrict/fast and stop all saturated fats you can reabsorb plaque. This would obviously be a challenge, I suspect autophagy plays a role in plaque reversal.
Hey Gil @nutritionmadesimple I couldnt find the video you mentioned at 37:12 "large fluffy ldls are harmless truth or myth". Can you post a link? Thanks. Dave
Thanks much, my questions are how often we see low or normal LDL cholesterol, while the Particle numbers are too high? and is it always in the context of presence of other illness like DM or other inflammatory disease? do we see this situation in healthy people having low LDL cholesterol and very high Apo B particle counts? thanks
Interesting info that explains in part how it is that people with normal LDL get heart attacks--Their particle number was high and never checked. So my layperson take away is...if your LDL is high it probably needs to be addressed. If your LDL is normal, get an ApoB particle test to make sure you're ok. Did I get that right? Neither my primary care doc nor my cardiologist do ApoB.
I'm not getting this particle versus cholesterol discussion. LDL for example is referred to as cholesterol and as a lipoprotein particle, sometimes in the same discussion. This makes statements like "cholesterol alone is not a good predictor of heart disease, it's the particle number that count" to be a real head-scratcher. Overall, this was great discussion, but the constant talk of "particles" was not helpful. Is it ApoB? I can't tell.
Dr. Cromwell does a very good job of laying out the mechanisms for plaque formation and cardiovascular disease. Excellent presentation, even though long. I would just add that most of these concerns can be sidestepped by simply eating a diet of whole plant foods. Automatically lowers numbers for cholesterol, etc., and has been seen to reverse cardiovascular disease (I've seen it in myself! :) ).
Huh. If particle count is the key predictor, then I wonder if degree of drop in cholesterol on taking a statin is an indirect measure of particle count. If you get a dramatic drop from the statin, then that implies that particle count was low under the assumption that the statin acts by adding receptors.
Correct. The LDL-Cholesterol measurement is a surrogate for measuring the particle count. It's somewhat imprecise and prone to discordance, but it's unfortunately mainstream's use. The better option, if you can't get particle count (LDL-P or ApoB), is to work with Non-HDL-C by subtracting HDL-C from total cholesterol.
Yes, I believe this is generally true. It lowers cholesterol and in the process of doing so, it decreases particle number without that necessarily being the precise target mechanism for how it works. Although for some statins like rosuvastatin (Crestor), it also has anti-inflammatory properties as well.
@hmbdata. The other mechanism of action of stations, besides upregulation of LDR receptors, is to inhibit the enzyme HMG Co-reductase that makes cholesterol in the liver. So I think it would be hard to tease apart overall reduction due to each factor as related to particle count
Yeah, that's an interesting question. It may vary from person to person and statin to statin, due to the percentage increase in receptors and the quantity of ApoB particles in your blood. As described by this video, my Doc had never heard of ApoB and I had to fight long and hard to convince him to test for it, but he eventually conceded. Came back at the highest end of the acceptable range whereas my LDL-C was very elevated, so I'm concentrating on getting my ApoB down now and tracking that. Next blood test in a couple of weeks so I'll be able to see how I've done.
As a layman, when hearing this type of discussion I'm constantly hearing references to inflammation but it's never explained or how it's detected. I assume it's not the same as what I may feel in my joints or muscles, etc. When I had a prostate biopsy my sheet showed (possible) inflammation in the numbers. I asked him what that meant, he said "I don't know". Any simple answer?
Isn't apoa1 more important than apob when your body releases enzymes to disolve triglyceride for use. Like you can use the energy and are left with excess ldl that needs to be transported away and if your apoa1 is low, that isnt going to happen and the exercise session can leave your blood with a lot of ldl with nowhere to go
ApoA1 is the most important but they don't mention it because there is no medicine they can sell to keep it in the optimal range which is above 150 mg/dL.
I would think that a large number of LDL particles would also suggest a smaller particle size as well. Because I did read which makes more sense to me where the much smaller LDL particles are the most dangerous kind and perhaps carry more of the Apo lipid B type proteins which apparently are more reactive or “stickier” so to speak and can lodge much easier between the epithelial cells that line the interior of an artery wall. Is this a true statement to assume? And are the smallest particles the most dangerous as well?
The number #1 lipidologist on earth! Bill is a great friend who I first listened lecture over 15 years ago. Excellent episode!
You can tell when someone REALLY knows their stuff - they are able to explain it so even nonprofessionals can understand the main points. They tread the fine line between glossing over and going too deep. Dr. Campbell really explained this all so well. Not saying I'll retain it all - but I have a much better understanding than I did before.
🎯 Key Takeaways for quick navigation:
00:00 🛡️ Cholesterol alone is not a strong predictor of heart disease events; it's the particle number that matters.
02:17 🎾 Cholesterol is transported in the blood via lipoprotein particles, like LDL and HDL.
06:17 🔄 LDL cholesterol and LDL particle count can disagree; risk is linked to particle count, not cholesterol levels.
10:11 💼 Discordance between cholesterol and particle number is common, especially in conditions like diabetes.
13:23 📊 LDL particle number, not cholesterol, significantly predicts heart disease events, especially with therapy.
16:32 🚀 Guidelines often aim for general population health; individual cases may require more nuanced assessments.
19:45 📋 Understanding individual risk factors, including LDL particle count, is crucial for personalized heart health.
22:41 🔍 Inflammation becomes more significant in advanced atherosclerosis, but it's not the primary initiator of plaque formation.
23:29 🩺 Chronic inflammatory conditions, like psoriatic arthritis, are associated with plaque formation due to arterial damage.
24:21 🩸 ApoB-containing lipoproteins, which contribute to plaque formation, move into the artery wall through a process called transcytosis.
25:31 🔧 The "response to retention" model suggests that once lipoproteins enter the artery wall, they need additional modifications to initiate plaque formation.
26:52 🚫 Triglyceride Rich Remnant particles are more atherogenic and contribute more quickly to plaque formation compared to LDL particles.
27:46 🧬 Type 3 Dyslipoproteinemia leads to the accumulation of atherogenic particles, causing rapid plaque formation.
29:03 🌊 Lowering LDL levels doesn't necessarily reduce all ApoB particles, and elevated triglyceride Rich remnants can still lead to heart events.
30:20 🩸 Modulating transcytosis or post-retention oxidation specifically is not currently possible. The primary focus should be on overall physiological health.
33:10 🛡️ Foam cell formation is the critical step in atherosclerosis. Reducing atherogenic particles helps prevent plaque formation.
35:03 📊 The risk of plaque formation depends on the concentration of lipoproteins that enter the artery wall, influenced by various factors like endothelial damage and lipoprotein levels.
38:04 🌱 Lifestyle changes, like managing blood pressure, glucose levels, cholesterol, and insulin resistance, are crucial for reducing plaque formation. More specific interventions are still under research.
Thank you!
Incredible! Thank you for summarizing so extremely well. This channel combined with good people like you literally make this a college level course on survival. Seriously, putting these pieces together over time is a roadmap for long life and healthy living. 👍👍👍
Thank you for this. Cheers!
Just use the chapters selection in the video description of each video. 🙄
After having read this summary & relating this current information to decades past information, a lot needs to be changed because they are already proven wrong.
Everyone should listen to this presentation. At least if not everyone, all cardiologists and primary care physicians should watch this. Incredibly informative and easy to understand. I sincerely hope that Dr. Cromwell will get invited back for a few more episodes.
Great video, Gil and Bill! My opinion may be a bit biased, but I'm a firm believer that EVERYONE needs to hear this conversation.
When I was going through chemo, and having regular CT Scans, they found two blockages. I talked to my Radiation Oncologist about it, and he said 'Not to worry'. I wish he had said 'Game on'. Maybe I would not have had the massive heart attack - maybe I would have changed my diet. I will admit to getting quite lost, watching this, but I will watch it a few more times, and pick up a bit more each time.
This is immensely valuable information conveyed in a very comprehensible manner. This channel is solid gold.
Would love to hear about how diet affects particle number
Great interview, but i wish that you asked dr. William what’s his thought of the right diet to prevent heart disease. Thanks
What a masterclass! Thanks for another great video Gil
What a great video. Often times we lose the nuance in medicine but Dr. Cromwell does a great job of explaining it. This needs to be required viewing for anyone who wants to take control of their own health.
You really need to be your own health advocate and this channel is a wonderful tool for that purpose. Thank you so much Dr. Carvalho!
38:22 Layman's explanation: Eat whole, non-processed foods instead of ultra-processed foods however and whenever possible. Don't overeat. Be active. Pass around five forks for one dessert. Don't smoke. Don't drink alcohol unless you can stop at one drink. Recent data is suggesting to just quit. That should be it.
Fantastic interview. Thank you! You are doing a phenomenal job educating the public. Had a couple of questions. 1. Is it only LDL particles stuck in the intima that can be damaged or can freely flowing LDL particles be damaged if exposed to glucose/insulin in the bloodstream. 2. Are all damaged LDL particles stuck in the arterial wall or can they come loose and get back into the bloodstream. 3. If damaged particles can get back in the bloodstream, can the LDL receptors on the liver still pick them up. 4. How do you balance the risks of lowering LDL particles with a statin versus the side effect of the statin (which may include causing diabetes), especially in the population that is low risk of getting plaque buildup even with a high apo-b count. 5. Does the triglyceride count and /or the insulin resistance increase risk of starting plaque formation (not increasing existing plaque formation which he said was almost certain).
Have you ever considered turning some of your content into a podcast? This is great info and I’d really appreciate it if it were in podcast format.
I've seen this type of request before and it confuses me. If you stop watching the video and only listen to it, don't you have a podcast?
@@darkpatches yes that’s what I usually do. But you have to pay RUclips to listen with video off.
@@paulgaras2606 Wow. YT just deleted my response comment and gave me a big personal warning about it. I explained how to get around the problems you have with the YT app. They're just plain mean and sore losers. I guess I can only tell you there are ways around it....
@@paulgaras2606 In regard to watching YT videos in a browser on your phone, I can only tell you to be brave. Be b r a v e.
@@paulgaras2606 No you don't. You simply play the video on your phone and listen to it on earphones or via the phone's speaker. I just did that very thing and it works fine (other than having to skip through the ads).
The information you provide on your channel helped me understand that I needed to reduce saturated fats, which brought my LDLc down by 25%. Thank you! Can't wait to see my Dr. in a couple days! Now as long as I'm not one of the ones where that's an inaccurate measure ....
Thank you Mr. Cromwell. The approach you take to the subject of Cardiovascular problems is scientifically honest without fanaticism, comprehensive and without placing yourself on any side of the conflicting parties
See...this is one of the more interesting topics I wish you could dive into....really need a 10 part series on this to break it all down
What else more do you want to know?
why don't we make things easy for everyone- just measure APOB as it tracks cause/risk better? not sure why we are still having this discussion. apoB test is like 30 bucks. why not run both?
Trying not to wear my tin foil, it's likely that there is just too much money to be made doing it the way they've been doing it all these years. I wholeheartedly agree with you though. Thanks to Dr. G, I learned that ApoB is a thing and had mine tested. It's extremely high, and diet and exercise has changed!!!!
what diet and statin and dose to reduce Apo(b)
@@randallcotner2155 Dr Sniderman
@@billusingh3439Every person responds differently. I only need 30mg Rosuvastatin to lower APOB from 129 to 59. Someone else may need multiple drugs, including expensive PCSK9 inhibitors, to achieve that. Talk to your doctor and experiment together.
Wow! The best video on the subject I've seen/heard. Please put the auto-translate in all languages captioning on for my non-english speakers like my wife who thinks all is fine. Thanks, dr. Carvalho & Cromwell.
This video, and this channel altogether, are so profoundly informative. Truly grateful Gil
Highest level info from the key experts, thankyou so much from Perth Australia
That was very nicely explained. Thanks. It reminds me of how BMI is an easy measure but not always the best measure.
Such a fantastic channel and interview. Second time I watched this. Dr. Cromwell is so lucid, you can't help but understand, and Dr. Carvalho's summary at the end helps to get you to the practical application of what you learned to protect your cardiovadcular health.
Very informative & most importantly very understandable! Much Appreciated! Thank You!
Just brought my wife home from the hospital after having a 95% blockage in one and 80-90% in another. Amazingly good cholesterol levels. Unfortunately, it is probably genetic and does tend to run in her family. But I agree, just the cholesterol numbers are not a very good predictor of heart disease. Total cholesterol was 147 and LDL was 72. Believe it or not they were going to put her on a statin. So far they haven't.
does she have high lp(a)? just a thought
Very interesting, educational, and informative. Many thanks for sharing Dr Carvalho
Brilliant interview, thanks Gil. Would love to know Dr. Cromwell's proferssional thoughts on HDL.
This channel is a gem!
I'm working my way through this very helpful video. I recently had blood work done in preparation for my annual physical, and asked if the could add an APoB test, thanks to Dr. Gil's videos. What I didn't know until after I'd had the blood drawn is that it takes a good week to get the APoB results back from the lab, instead of the normal 24-48-hour turnaround.
Great video.
After I finish it I will check your other videos about it and saturated fat that I watched but didn't grasped fully.
Good explanations.
I think now I got it more fully.
Look for the book Nourishing traditions. It's an older book but really explanatory and good information
Very interesting and informative discussion. Thanks 😊
Thanks that cleared up a lot of misunderstanding about heart disease.
The lifestyle measures of heart disease risk:
1) Are you overweight? (BMI above 25): No.
2) Do you get angry when I ask what your waist measurement is? No.
3) Do you smoke at all? No.
4) Do you drink more than very occasionally? No.
5) Do you eat a plant *biased* diet with the majority of your calories coming from whole (high fibre) foods? Very low in saturated fats. Yes
6) Do you exercise; about 5 hours a week *brisk* walking with hills and stairs or equivalent plus some weight/isometrics? Yes.
That covers all the practical things you mention in your other videos.
My theory is most people who are obsessed with biomarkers are trying to find a reason those questions don't apply to them!
I don't know about most people but I don't fit the normal model of a high risk person (no family history of early events, never smoked, BMI of 22 and regular exercise for many decades, no symptoms, etc.) so when I got a "severe" coronary artery calcium scan, biomarkers became the way to measure my progress in reducing risk. Hopefully that's what other people who're smart enough to watch this video are doing with them also.
@@dwights1464 What are you doing to reduce your risk that isn't on my list?
@@RogerHyam I have been taking rosuvastatin for about 3 1/2 years and Zetia for about 3 years to lower my risk.
@@dwights1464 and have you been on a wholefood, plant based diet for most of your life?
In my original point I say *most* people are trying to get out of one of the items on the list and you haven't said you have done all the things in the list - plus you might not be *most* people.
Such a beautiful and wise conversation
I've decided that every expert has valid points. Every meta study has valid assertions. Every individual has to realize that neither of those two facts mean much to their particular health condition. It is a roll of the dice because of too many unknown factors in our bodies.
Who needs a heart ❤️ when a heart ❤️ can be broken 💔? 😶
- Dr William Cromwell is a clinical lipidologist, professor at Wake Forest University School of Medicine, and he has published many studies on lipid physiology and metabolic disease.
10:05 chapter on the discordance between LDL-C and ApoB: he said that 30-50% of healthy people have such discordance, while metabolically unhealthy people are more likely to have discordance (up to 70% of them have it). he also says there is no discordance when LDL-C is very high or very low.
Discordance is not essential. Have low LDL-C, low blood pressure, low inflammation, low blood glucose and you are safe.
Sad to hear this info cant go mainstream because the old view of cholesterol is too deeply lodged into our healthsystem.
Thanks for these type of videos, greatly appreciated to get information from suxh a knowledgable person
Gill, did your views on atherosclerosis change as a result of this interview?
Thank you Gil! So glad i subscribed. You are a solid channel!
Despite eating a plant based diet and exercising frequently I discovered through advanced screening that my risk for diabetes and heart disease is higher than I expected and much higher than I want. I am currently using fiber supplementation and sodium reduction to reduce my risk and then I am going to re-test. I already noticed that my blood pressure has come down since I started the interventions. I'm very excited to see how well these interventions have worked to reduce my risk but I'm trying to wait because the testing is fairly expensive and I want to give it time to work.
Try switching to a WFPB (if you don't practice it already) and try using very little salt, or using combinations of sodium-free salt and sodium-containing salt. You can find more information about this on Gil's video on the best salt for health, where he discusses a sodium-free version of salt. Read the comment section on the video too, people there had good suggestions.
Diet and exercise aren’t everything. Emotional wellbeing is HUGE and very overlooked.
Good work on adapting! I had to do the same thing, even though I was eating a whole food plant based diet like you, I ended up having to exercise more, get rid of ground grains from my diet (bread, pasta, etc), potatoes, and salt. I also added some potassium chloride. With these changes, over the course of a few months my numbers moved into optimal range.
@@Teneab thanks I already try to eat WFPB for the most part but the junk creeps in. Part of the intervention is trying to avoid the plant based junk as well. I’ve been using a 50/50 blend of potassium chloride and salt and using less of that overall. I have lost weight and I feel like I’m really on the right track. Wishing you good health!
@@bgrune1 Oh sounds like you are already doing everything correctly, lol! Keep up the great work. Have you checked your ApoB or cholesterol since you've started the intervention?
Hello Doc: can you share your diet and lifestyle (sleep, exercise, anything else important) for good health? Since you have researched a variety of topics over the years, I imagine you follow some best practices. Thank you so much
Secret
Whole food plant based. No coffee. Decaf only. No fat.
Look 37:46
@@kate60 no fat ?!? Maybe you mean no animal fat but you need some fat in ur diet xd
While this is an interesting conversation, I'm not sure how useful it will be to the average viewer. I appreciate the technical explanation of why measuring cholesterol isn't perfectly accurate to every individual, but I don't know how to apply this information to a real-life scenario. Basic information on how to manage the potential risk factors (like exercise, smoking cessation, drinking cessation, lowering cholesterol, etc.) would be more practical for me. In what way does the information presented here change the advice given to the general public? If someone were to ask me what causes heart disease, I wouldn't know how to translate this information in a way for them to practically understand.
good question. the general knowledge to heed high glucose, blood pressure or cholesterol levels is directionally correct but can miss risk factors in many people, hence knowing insulin resistance metrics, ApoB or nonHDL-cholesterol can provide more information. also see some of our previous content on heart disease where we touch on a lot of the basics like diet tips, lipid panel etc. In response to that, many viewers asked for more detailed videos on the mechanistic & molecular aspects and that's what this series partly aims to cover
Thanks, that helped to clarify a lot of the misunderstandings I was having. So this is just more accurate information that we can use to in order to assess hidden risk factors.
This was a fantastic and informative interview, thank you for this!
So ApoB is a good predictor irrespective of LDL is what is being implied, yes?
Absolutely yes.
Where has he been? Love the info, but what about specific numbers of what is too high, target numbers? what about any of the usual ratios? & What about HDL, Triglycerides, & ApoA?
Dr. Cromwell is a great doctor. However, it would be great if Dr. Cromwell would continue to treat his patients that are dependent upon him to answer questions and fill prescriptions.
Hi Gil, here's a thought. How about a podcast on how to individualise health guidelines?
Great episode Gil!
My insight about this metabolic problem with the foam cells etc is that some prolonged fasting could be an amazing method to prevent issues.
This was amazing! One of the most informative explanations
But will your insurance pay for the scan? I received a scan from my cardiologist who found nothing after an odd EKG and strong echo; 6 weeks later I had my heart attack and got 4 stents. The term 'worthless" comes to mind.
Thanks so much for the video. I've been plant-based for 11 years now and have listened to Drs Esselstyn and Greger to get my LDL below 75 and total cholesterol to below 150. So now I need to make sure my apoB is below 100 mg/dL? Thanks Gil!!!
I'm from a family w catastrophic heart attacks, high blood pressure, and very high cholesterol which IS added to by diet.
I however have very high cholesterol (yhe highest was almost 400 LDL).
On pravastatin as it doesn't cause brain issues or joint and muscle pain. Down to almost satisfactory levels by medical standards, but too low (ideal level) is brain foggy and memory issues.
No calcium in heart also.
I'm about finished with worrying about my cholesterol and trying to get it lower.
No heart issues at this time, and those who had catastrophic heart attacks or issues were already showing problems before they died
I flat out told my doctor that I wanted him to order an ApoB test and his response..."We don't do that unless there is a problem.'
Like what?!? He can order whatever tests he wants for me and why does he care what test that I want done? I am paying for it and all it does is give him more information.
Because I asked for it he won't do it?
Ok, so what if a lipid panel came back with numbers that he didn't want to see and then he calls me back in to get the ApoB that I asked for? That is literally a couple hours of time on my part, another blood draw, etc. If I was working, that would be more time that one would have to take off of work.
Very inconsiderate at the minimum. What doctor would care if you ask for some benign test that simply uses some of the blood that they are already drawing from you?
great video - amazingly educational. questions: is there a way to reduce plaque if it is formed and can grow? habitual, dietary not intervention ways.
similarly = what we can do to lower APO-B?
Excellent show full of useful info.
Hi Gil. I love your videos and subscribe to your channel. Thanks. I would really like to hear your opinion about the new abstract from March 18, 2024 from the American Heart Association: "8-hour time-restricted eating linked to a 91% higher risk of cardiovascular death". It's hard to know what's right and what's not these days.
Love the bottle of scotch on the desk - must be fortification for the incomming denier/inflammation deluge - always excellent …
lol I think it’s a green screen backdrop. But that is funny.
Hey, can you please consider making a video on Chonline, the possible deficiency of it in lacto-vegetarians and vegans and how those two groups can have sufficient levels?
PS: Again, posted this on twitter too but again I have doubts twitter is working properly or may be censoring tweets for some reason.
Fantastic video! Dr. Cromwell says at 25:30 that "once you're in" it's not guaranteed that you'll "stir the pot and cause problems." Does this mean that oxidization has some specific cause? Or is it entirely that certain types of particles get oxidized and others don't? Asked another way - is it the particle type that determines retention + oxidization, or are there other mechanisms that cause more retention and oxidization?
Great talk. Thanks for putting in that list of references!
Fascinating stuff
This is only one aspect or type of heart disease. What about arrhythmias? Afib is common in older people. Why? What causes it? Can it be prevented?
You can prevent it with a pacemaker.
You cannot prevent arrhythmia with a pacemaker. A pacemaker just lowers hb per min. Some people have episodes of afib...but when not in afib their hb is very low already. That is why ablation is the no 1 procedure for afib...but it doesn't always work.
@@betzib8021 thank you for your explanation :)
What about the importance of keeping the functionality of HDL to improve cholesterol efflux? How can the fonctionality of HDL be increased? Also I would have liked to know if lowering LDL a lot doesn't lead to problems in other tissues? Some say that going as low as possible is ok, is it true? It seems for instance than in old age people need more LDL.
I'd also like an explanation as to why LDLs only cross the endothelium at a single site (the plaque site) rather than spreading out along every centimetre of artery wall. After 4 million years of evolution, you'd have thought that we would mitigate the problem of atherosclerosis by spreading out the problem over the entire blood system rather than focussing in on a few discrete spots until they become inflamed and rupture. It can't be a coincidence that plaques more ofter occur at branches and confluences in the arteries, more prone to damage caused by eddy currents, high pressure and abrasives.
there is ongoing research trying to investigate further this site specificity, see ruclips.net/video/0u0K97ty8xs/видео.html
What should patients do? I’m trying to get my brother to the doctor. He has a huge gut, fat face, and we have diabetes in both sides of our family. Do doctors get upset if you come in and ask for tests? My numbers are ok, says my doctor, but I know I have a problem too because my blood sugar goes up when I eat certain foods. Thanks Docs, both of you, for sharing your knowledge.
The way I look at it is with this formula:
(Non-HDL-C / Amount of atherogenic particles) = average particle size.
Since ApoB measures the number of atherogenic particles, let's separate it in the formula, and we get:
ApoB = (Non-HDL-C / average particle size).
So, to optimize ApoB, we should try to optimize two things:
1. Reduce Non-HDL-C
2. Increase particle size
Looking at Non-HDL-C is just half of the equation.
So, my question is: As lab tests can already measure Non-HDL-C, and most people don't have access to ApoB measurements, how can we estimate the average particle size by other results and determine if Non-HDL-C is an accurate representation of our risk?
Why do you think “most people” can’t get an ApoB?
As long as you can count the number of particles, the particle size is not predictive of ASCVD events. The misnomer of "small dense & "big fluffy" boils down to: "where there are a lot of them (particles) crammed into the same space (unit of blood), then they are more dense (smaller)." Getting insulin sensitive AND reducing particle number is the name of the game.
@victoriaboster1177 I don't. Maybe I should have written "some people", anyway I can't
@mattbmartin Seems like you did not understand clearly what I wrote. The average particle size does matter but not as a single measurement. It should be combined with Non-HDL cholesterol since together they can predict ApoB
@@lotembenatar7163 Particle size is not relevant to risk because all atherogenic lipoprotein particles are small enough to get into the arterial wall.
Fantastic information, thank you both.
Dr . I take Burlinta and I have one stent in my arteries . But I work out daily and eat very healthy can I stop taking Burlinta . I feel strong and healthy now
36:42 When contradictory knowledge and findings are accepted as valid, then we may have to think of a new model to accommodate these different results. This reminds me of a similar dilemma in the world of Physics, and how I learned in physics class that light can be described both as a wave or as discrete particles. I was told that someday a new model might be developed that accommodates both theories of what light really is. But I digress.
Can someone explain to me something, please: I understand the notion of measuring cholesterol versus particle count, especially the ApoB marker for seeing how many lipoprotein transporters there are. I understand that these transports can be packed full of cholesterol/triglycerides, but what triggers the creation of lipoprotein carriers themselves? Does the body make more to respond to excess cholesterol/triglycerides in the blood?
Yes; no excess cholesterol/triglycerides(i.e. fats), no need for the body to make ApoB. ApoB is there just to wrap around cholesterol/triglycerides and help them dissolve into the blood (which is mostly water), since they (fats) are unable to do so by themselves.
So given the dr ‘s answer, why would there be discordance where there is low cholesterol but high ApoB?
Awesome video and great interview!
Fantastic explanation of lipoproteins
Excellent
This might be a stupid question. But can you please explain (in a scenario where APO-B is high and LDL is low) how that leads to cardiovascular disease? To explain my question, I will use this analogy. Let's say I have 10 people with bad intentions that want to get from point A to B to cause harm. And, there are 100 cars available to transport them with each car able to transfer one person. Once all ten have been transported, the remaining 90 cars on their own can't cause any harm as there are no more ill intentioned passengers to transport. They are empty. But not for the cars, there would be no harm done at point B. But, if there are more cars than bad intentioned people, how do the cars cause more harm? Thanks for the great video. It would just be great to have a better understanding of the actual numbers of APO-B vs LDL in a situation where LDL is low and APO-B is high. Thanks again!!!
It´s rarely discussed one of the most important metrics of health, possibly the most. The omega 3 to omega 6 ratio in your tissues, ideally 1:1 and even 1:3 is within healthy range. Balance is key. If your omega 3 is low you´ll have to tightly handle your omega 6 s. If your omega 6 s are through the roof you´ll have to push your omega 3 through the roof. Some believe that omega 3 s are magic pills that will make all your body problems evaporate. They are not, but still very helpful.
I enjoy these interviews with lipidologists. Because of the last few I've seen, I have gone back on a statin. I have low bmi, zero calcium cacs.....etc etc. My remnant cholesterol is extremely low, but after learning that the number of particles is a driving factor, I decided to make this change. It would be good to see a video explaining apo b and ldl particles. Is apo b the size of the ldl particles? If that's the case, mine are the fluffy A ones based upon all other information.
ApoB is the mass (remember mass is independent of the force of gravity so your mass is the same on Earth and the Moon) of the ApoB containing particles in a deciliter of blood. The units of measure are mg/dl. It is my understanding that LDL particle number is a numerical count of LDL particles. The units of measure are nanomoles per liter of blood. One mole is 6.022 times 10 to the 23rd power. A nanomole is one billionth of that.
He says at the end if there's plaque, it's time to "shut it down." Well, how does one do that?!
Doing all of the things that prevent plaque formation will also help stabilize existing plaques.
@@megavegan5791 What are all the things that prevent plaque formation? Is it just not eating saturated fat?
@@southerngirl1408First and foremost, get ApoB down to a healthy level, either through diet & lifestyle, prescription medication, or both.
@@southerngirl1408prevention of lactic acidosis and it’s progression to chronic inflammation.
is there a rate of clearance of atherosclerosis? in other words, is our body able to clear a little bit of atherosclerosis over time, if health parameters are optimal? in other words, is atherosclerosis in a constant dynamic equilibrium between clearance and accumulation?
Google what happened in Norway in 1940, mortality from circulatory diseases. When Germans occupied Norway, they sent all meats and dairy products to the eastern front, in effect turning Norway vegan. It resulted in a nearly instantaneous 20% drop in cardiac/stroke mortality. The coroners saw these shadowed areas in the arteries of deceased Norwegians that were, they think, where plaques once were present. It would appear if you calorie restrict/fast and stop all saturated fats you can reabsorb plaque. This would obviously be a challenge, I suspect autophagy plays a role in plaque reversal.
Hey Gil @nutritionmadesimple I couldnt find the video you mentioned at 37:12 "large fluffy ldls are harmless truth or myth". Can you post a link? Thanks. Dave
So how does one go about lowering or decrease # of particles? I feel this most important ? was missed.
Eat more fiber and more plant Protein and less saturated Fat
Your channel has excellent content. Thank you for this. I can forgive the fact that you look like Liza Minelli and Ralph Machio's love child.
Thanks much, my questions are how often we see low or normal LDL cholesterol, while the Particle numbers are too high? and is it always in the context of presence of other illness like DM or other inflammatory disease? do we see this situation in healthy people having low LDL cholesterol and very high Apo B particle counts? thanks
Interesting info that explains in part how it is that people with normal LDL get heart attacks--Their particle number was high and never checked. So my layperson take away is...if your LDL is high it probably needs to be addressed. If your LDL is normal, get an ApoB particle test to make sure you're ok. Did I get that right? Neither my primary care doc nor my cardiologist do ApoB.
I'm not getting this particle versus cholesterol discussion. LDL for example is referred to as cholesterol and as a lipoprotein particle, sometimes in the same discussion. This makes statements like "cholesterol alone is not a good predictor of heart disease, it's the particle number that count" to be a real head-scratcher. Overall, this was great discussion, but the constant talk of "particles" was not helpful. Is it ApoB? I can't tell.
So good! Thank you very much
Great information. Thanks
Dr. Cromwell does a very good job of laying out the mechanisms for plaque formation and cardiovascular disease. Excellent presentation, even though long. I would just add that most of these concerns can be sidestepped by simply eating a diet of whole plant foods. Automatically lowers numbers for cholesterol, etc., and has been seen to reverse cardiovascular disease (I've seen it in myself! :) ).
Excellent. Very clearly explained. Thanks to both ❤
Hi what I would like to know how do you lower inflammation?
Have you looked at the function of the glycocalyx. Not many people talk about it.
Now the real question is if high cholesterol foods tend to raise APO-B in the context of an otherwise good quality diet.
Huh. If particle count is the key predictor, then I wonder if degree of drop in cholesterol on taking a statin is an indirect measure of particle count. If you get a dramatic drop from the statin, then that implies that particle count was low under the assumption that the statin acts by adding receptors.
Correct. The LDL-Cholesterol measurement is a surrogate for measuring the particle count. It's somewhat imprecise and prone to discordance, but it's unfortunately mainstream's use. The better option, if you can't get particle count (LDL-P or ApoB), is to work with Non-HDL-C by subtracting HDL-C from total cholesterol.
Indeed, statins will lower your apoB. I am on a statin and my apoB is 0.37 g/L (normal range 0.59-1.25).
Yes, I believe this is generally true. It lowers cholesterol and in the process of doing so, it decreases particle number without that necessarily being the precise target mechanism for how it works. Although for some statins like rosuvastatin (Crestor), it also has anti-inflammatory properties as well.
@hmbdata. The other mechanism of action of stations, besides upregulation of LDR receptors, is to inhibit the enzyme HMG Co-reductase that makes cholesterol in the liver. So I think it would be hard to tease apart overall reduction due to each factor as related to particle count
Yeah, that's an interesting question.
It may vary from person to person and statin to statin, due to the percentage increase in receptors and the quantity of ApoB particles in your blood.
As described by this video, my Doc had never heard of ApoB and I had to fight long and hard to convince him to test for it, but he eventually conceded.
Came back at the highest end of the acceptable range whereas my LDL-C was very elevated, so I'm concentrating on getting my ApoB down now and tracking that.
Next blood test in a couple of weeks so I'll be able to see how I've done.
Are there treatments for apob that is out of range? If not, testing for it won’t matter.
That first 5 minutes must be the worst answer to the question " what is heart disease to the Lay Man". Talk about esoteric????
As a layman, when hearing this type of discussion I'm constantly hearing references to inflammation but it's never explained or how it's detected. I assume it's not the same as what I may feel in my joints or muscles, etc. When I had a prostate biopsy my sheet showed (possible) inflammation in the numbers. I asked him what that meant, he said "I don't know". Any simple answer?
Isn't apoa1 more important than apob when your body releases enzymes to disolve triglyceride for use. Like you can use the energy and are left with excess ldl that needs to be transported away and if your apoa1 is low, that isnt going to happen and the exercise session can leave your blood with a lot of ldl with nowhere to go
ApoA1 is the most important but they don't mention it because there is no medicine they can sell to keep it in the optimal range which is above 150 mg/dL.
I would think that a large number of LDL particles would also suggest a smaller particle size as well. Because I did read which makes more sense to me where the much smaller LDL particles are the most dangerous kind and perhaps carry more of the Apo lipid B type proteins which apparently are more reactive or “stickier” so to speak and can lodge much easier between the epithelial cells that line the interior of an artery wall. Is this a true statement to assume? And are the smallest particles the most dangerous as well?
we have another segment of this interview coming soon exploring this question of particle size in detail. hopefully we'll release in a couple weeks
@@NutritionMadeSimple Will the LDL-C to ApoB ratio be discussed as an approximation of particle size?
How does vitamin D impact this as it is an inflammation modulator?
fantastic information!