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.
🎯 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.
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.
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.
@@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).
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).
- 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.
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 ....
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.
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
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.
Whats her APO B???? How about LPa?? How about HS-CRP? Lastly and most important, whats her LDL particle number?? LDL and HDL are current day bullshit...But most docs have their heads up their asses regarding 99% of current findings and tests.
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.
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'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.
7:40 If particle number is low but LDL is high, risk is low. It’s the particle number (not cholesterol) that forms plague. 10:34 discordance between LDL cholesterol and the actual number of particles can be as much as 75% with factors like diabetes, insulin resistance, and metabolic syndrome. So, Dr. Ovadia being on your channel and speaking about who ends up on his operating table makes a lot of sense. He obviously sees a lot of people with those issues who have lower LDL cholesterol and a 75% discordance would make anyone determine that cholesterol was a not so reliable marker of heart disease. At 11:00 in, “75% discordance is encountered pretty commonly.” “On a good day, it’s” a toss up and “on a bad day, it more likely to be wrong, than right.” 12:38 looking at the low and high extremes of LDL cholesterol and participle number are more likely to have concordance. Thereby, docs just use LDL cholesterol as the marker, however that ignores that between those two extremes there’s far more discordance. 17:20 LDL cholesterol as a marker “isn’t bulletproof. It’s a poor guesstimate.”
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.
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?
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
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.
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?
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
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.
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
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?
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!!!
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?
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.
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.
Love the scientific way you go about proving what you say. Great channel. Does atorvastatin and rosuvastatin target cholesterol or Apo(b). My cholesterol LDL has been high since my 20's. been on low dose statin for 40 years. Still not low. Only time my LDL was below 100 was the 8 months on Atkins where i ate nothing but steak, cheese sauce and eggs. Lost 80 pounds. Cholesterol plummeted. HDL has always been low. My doctors could never answer why it dropped. At 60 my calcium score in chest was 0. Is there something else i should be checking.
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.
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.
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.
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.
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.
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
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.
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.
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?
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.
Could some particles that have already entered the subendothelium exit back to the lumen?! If so how is that, n if not it means transcytosis inevitably leads to retention!.
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.
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.
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.
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.
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?
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?
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.
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.
What does he mean by "remnant triglycerides?" Do remnant triglycerides show up in your normal lipid blood tests? And he has a company that custom looks at the various factors (APOB, particle number, remnant trigs etc) his research feels is most pertinent? If so what are those parameters and how might we get access to that type of testing?
@@nanduthalange7736 So it means triglycerides that do not show up on a normal lipid test? And they are able to be calculated from other parameters? (HDL and "regular" trig levels?) How do you know all this? What qualifications do you have?
Very informative but what are the next steps? This was good information, but what can a person do in regards to lifestyle to get their LDL particle down and their APO B? Any particular diet or lifestyle change?
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
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.
🎯 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.
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.
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.
Not to worry? 😮
I agree I’m totally lost.
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.
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
What a masterclass! Thanks for another great video Gil
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 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.
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 UA-cam 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).
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!
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).
- 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.
This video, and this channel altogether, are so profoundly informative. Truly grateful Gil
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 ....
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?
This channel is a gem!
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.
Highest level info from the key experts, thankyou so much from Perth Australia
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.
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
Brilliant interview, thanks Gil. Would love to know Dr. Cromwell's proferssional thoughts on HDL.
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
Whats her APO B???? How about LPa?? How about HS-CRP? Lastly and most important, whats her LDL particle number?? LDL and HDL are current day bullshit...But most docs have their heads up their asses regarding 99% of current findings and tests.
Such a beautiful and wise conversation
Awesome video and great interview!
That was very nicely explained. Thanks. It reminds me of how BMI is an easy measure but not always the best measure.
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.
Thank you Gil! So glad i subscribed. You are a solid channel!
Very informative & most importantly very understandable! Much Appreciated! Thank You!
Very interesting, educational, and informative. Many thanks for sharing Dr Carvalho
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.
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.
This was amazing! One of the most informative explanations
How does diet affect particle numbers?
Gill, did your views on atherosclerosis change as a result of this interview?
7:40
If particle number is low but LDL is high, risk is low. It’s the particle number (not cholesterol) that forms plague.
10:34 discordance between LDL cholesterol and the actual number of particles can be as much as 75% with factors like diabetes, insulin resistance, and metabolic syndrome. So, Dr. Ovadia being on your channel and speaking about who ends up on his operating table makes a lot of sense. He obviously sees a lot of people with those issues who have lower LDL cholesterol and a 75% discordance would make anyone determine that cholesterol was a not so reliable marker of heart disease. At 11:00 in, “75% discordance is encountered pretty commonly.” “On a good day, it’s” a toss up and “on a bad day, it more likely to be wrong, than right.”
12:38 looking at the low and high extremes of LDL cholesterol and participle number are more likely to have concordance. Thereby, docs just use LDL cholesterol as the marker, however that ignores that between those two extremes there’s far more discordance.
17:20 LDL cholesterol as a marker “isn’t bulletproof. It’s a poor guesstimate.”
So ApoB is a good predictor irrespective of LDL is what is being implied, yes?
Absolutely yes.
Very interesting and informative discussion. Thanks 😊
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.
Excellent show full of useful info.
This was a fantastic and informative interview, thank you for this!
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?
Fantastic information, thank you both.
Thanks that cleared up a lot of misunderstanding about heart disease.
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
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.
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?
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
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
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
Who needs a heart ❤️ when a heart ❤️ can be broken 💔? 😶
What doesn’t kill you makes you stronger, right?❤
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?
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!!!
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?
Hi Gil, here's a thought. How about a podcast on how to individualise health guidelines?
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.
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.
Fascinating stuff
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.
Love the scientific way you go about proving what you say. Great channel. Does atorvastatin and rosuvastatin target cholesterol or Apo(b). My cholesterol LDL has been high since my 20's. been on low dose statin for 40 years. Still not low. Only time my LDL was below 100 was the 8 months on Atkins where i ate nothing but steak, cheese sauce and eggs. Lost 80 pounds. Cholesterol plummeted. HDL has always been low. My doctors could never answer why it dropped. At 60 my calcium score in chest was 0. Is there something else i should be checking.
Great talk. Thanks for putting in that list of references!
Excellent
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
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.
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?
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.
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.
Can there be discordance between ApoB and non-HDL?
As far as I know, yes, they can be discordant because Non HDL-C is a measure of cholesterol amount, not number of particles.
Fantastic explanation of lipoproteins
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 :)
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
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.
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.
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.
Does diet play a part in heart disease and if so what foods cause it?
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?
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.
Could some particles that have already entered the subendothelium exit back to the lumen?! If so how is that, n if not it means transcytosis inevitably leads to retention!.
yes, most circle back, only a minority gets retained
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.
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.
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.
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.
fantastic information!
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?
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?
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.
Are ApoB tests more expensive than HDL/LDL? Does triglycerides and HDL/LDL information predict ApoB?
How do you measure particle number?
Ask for an Advance lipid test, called a NMR.
Does apoB measure particle number?
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.
How do I know I have inflammation and if so to which extent is it critical?
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.
What does he mean by "remnant triglycerides?" Do remnant triglycerides show up in your normal lipid blood tests? And he has a company that custom looks at the various factors (APOB, particle number, remnant trigs etc) his research feels is most pertinent? If so what are those parameters and how might we get access to that type of testing?
Triglycerides in chylomicron remnants and VLDL remnants/ IDL
Indicated by high triglycerides and (usually) low HDL-C
Squatters.
@@nanduthalange7736 So it means triglycerides that do not show up on a normal lipid test? And they are able to be calculated from other parameters? (HDL and "regular" trig levels?) How do you know all this? What qualifications do you have?
Great information. Thanks
25:00 No, you can no "wiggle" between the cells.
Very informative but what are the next steps? This was good information, but what can a person do in regards to lifestyle to get their LDL particle down and their APO B? Any particular diet or lifestyle change?
see ua-cam.com/video/18FF4pYLxek/v-deo.html
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