Such a nice person tom is.. I am a physician and i Learned a lot from him.. My whole thinking has changed regarding lipoproteins and CV risk. Thanks peter for such great podcasts.
I've studied many scientific topics and came accross lipidology fairly recently, and I don't know why I've never been excited as much as I am about lipids... So for me it's no surprise your podcasts on lipids are a hit!
I'm not a physician, just a patient trying to understand my own lipids and risks. I was disappointed that in this entire interview, not one single mention was made of studying and changing the patient's dietary intake of macronutrients which are the inputs into the lipid metabolism. For example, if someone has extremely high triglycerides, instead of using a drug to lower that, shouldn't the first line of treatment involve altering the lipids and carbohydrates in the diet?
Because they want people to take statin? There are keto/LCHF diet that would effectively lower Triglycerides for most people, but might increase LDL (and APO-B) for some.
I think there just isn't one answer to that question. People respond differently to different approaches.. I lowered my TG from 170 to 53 in a couple months by switching to LCHF, but my LDL went up 40%. You don't know until you try.. tweak, analyze, assess, repeat.
My LDL-C went up too, when I did a LCHF diet pattern of eating. My doctor was concerned, but I wasn't because I had studied that LDL particles that are large don't cause atherosclerotic plaques. It's the small dense LDL particles that are atherogenic. My ratio of TG/LDL-C, which was 2.0 (in American units), indicated that nearly all of my LDL was not atherogenic. @@SwoleTown Watch A/Prof. Ken Sikaris - 'Making Sense of LDL' ruclips.net/video/2p-mkbNutvQ/видео.html and this link jumps to the part of another lecture where Dr. Mason explains how to tell if your LDL are large (pattern A) or small (pattern B) from standard lipids tests: ruclips.net/video/DXKJaQeteE0/видео.html .
Thank you Peter and Tom for giving so generously of your time to make these very detailed and inforrmative podcasts which instruct the world. They are so so helpful. I am very grateful.
Listening to Peter's vids have made me way more critical whenever I listen to other people discuss health and wellness. More often, when watching other videos, I find myself saying, 'ehhhh, Peter Attia would likely stop you right there and have something to say' lol. That's good though, because even if one doesn't fully understand a topic, it's good to at least know when to start being critical. Like when statistics or any kind of number are being cited
Had a cardio IQ panel from quest come back with phenomenal numbers in all categories from a standard lipid panel as well as apob and LP(a), but LDL-P was high risk. My question was how can apoB be low while the particles that contain apoB were high? Discordance among the "same" particles. Thank you for clarifying that NMR can be inaccurate for LDL-P and that apoB should be the metric for risk when discordance is seen between these metrics! What a headache trying to track this down haha
I just got really confused...you asked him about the effects on Lp(a) from statins and other drug and he started talking about ApoA...aren’t they two totally different things? I’m lost...
Dr. Attia, Please consider: if arterial schelorosis is the result of an inflammatory response. As insulin resistance increases, increased glucose damages the arterial wall, allowing cholesterol to enter the arterial wall. Reduce insulin levels, reduce arterial plaque. Am I headed in the right direction?
While I've enjoyed and been greatly informed by your podcasts, the lipid series are frankly confusing, scattered and poorly organized. This is especially true of this last one. I think it's confusing because lipidologists haven't figured out the mechanism for atherogenesis and therefore haven't really figured out what and how to measure. It would have been better organized into Rumsfeld's knowns, unknowns, known unknowns and unknown unknowns.
@@ucchi9829 I thank you for your remark as it led me to find supplementary resources: here is one from Dayspring and it's a very clear exposition in PPT form: ruclips.net/video/89QEoUaxiDo/видео.html&ab_channel=TrueHealthDiagnostics and is an oldie but goodie from Peter Attia re cholesterol: peterattiamd.com/the-straight-dope-on-cholesterol-part-iv/
@@gondwana6303 Attia's take #7 is wrong but I think there are better posts/reviews on this topic. I'll link you a video and current literature: ruclips.net/video/wJKqq3ERLFs/видео.html Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel academic.oup.com/eurheartj/article/41/24/2313/5735221#198921792 The Role of Lipids and Lipoproteins in Atherosclerosis MacRae F Linton et al 2019 www.ncbi.nlm.nih.gov/books/NBK343489/#_NBK343489_pubdet_
My Lp(a) is always rock bottom low (3 nmol/L or 1.34 mg/dl) but even on a ketogenic diet long-term (15 years) I have to take niacin to lower my triglycerides.
If you have a PCP who orders routine blood tests for you, Trigs OUGHT to automatically be included along with HDL and LDL PARTICLE SIZE, Good luck-tit will really help to know those figures. 😋👍
39:27 If HDL isn't a significant factor in predicting disease, then is the TG/HDL ratio now mostly useless? And if useless, what data is most useful from an average cholesterol report.
The ratio is useful it's not as sophisticated and up-to-date dr.day Springs level understanding. What is most useful is Apo B. Apo B is part of LDL if LDL is not super high they both correlate. Also get a one-time test for Apo little a. It is pathological and not everybody has a pathological level of it.
I think it's very useful, and as he stated, it's the "why" that matters.. why are TG high and HDL low? probably because you're insulin resistant. That, then, can lead to dramatic increases in ApoB, slower clearance rates, increased chances of atherogenesis.
At the 23:05 mark, you mentioned that you have a patient at your practice with total cholesterol of 300 and LDL 220 APO B 170 but her CAC is zero. Did you check her soft plaques? Maybe there are many more exceptions like her? Maybe APO B is not such a good CVD indicator? What is her triglycerides to HDL ratio?
But when you're first responders are being forced to carry torches and gasoline, which they set down at every scene, they're also a problem. Of course the answer is to stop the source of torches and gasoline, not to fire all first responders.
@@Unsensitive but that’s not necessarily the context which the blood lipid conversation, and specifically LDL, is being painted by the vast majority of those who still carry a torch for the old health heart hypothesis and ultimately the wide scale dispensary of statins.
I don't think that's what's being stated here, or in the entire 5 part series. In fact, it's stated multiple times that LDL isn't a great marker, and that ApoB should be used in it's place going forward.
@@wmartonejr apoB/LDL has been proven to be causative of cardiovascular disease through numerous different mechanisms of sample sizes of hundreds of thousands in prospective cohort studies, randomised controlled trials and Mendelian randomisation studies which all show the same thing. No one is basing it off mere association. It’s proven in the outcome data that lowering LDL causes massive reductions in all cause death.
Sometimes people have the correct knowledge, but do not, for whatever reason, implement it well in their own life. It is easier to say what to do than to actually do it. The content is more important than the messanger or the delivery, but most people have been taught to trust information based on the credentials, authority or delivery of the presenter.
@@wocket42 the fact that he is overweight has nothing to do with whether is information is of no use or academic in nature only. I don't think that all of his lipoprotein babbling is of any practical use, but the initial comment had to do with a logical fallacy of judging the nature of the content on the appearance of the presenter. That type of logic is why people think that the stuffed shirts of corporate media are authoritative.
@@ucchi9829 CAC of zero is a strong indication that you are not at risk. Of course, it is not fool proof, but if you have good lipid profile (2:1 ratio of hdl/trig) and a zero CAC score, I personally would not touch a statin
@@museitup4741 the literature on CAC scores is weak first of all. Second, on the clinical side, they are only considered in very specific scenarios.... if you fall into the low risk category and you’re around 40+ you can talk to your GP to see if it’s worth considering. A CAC score doesn’t reflect what you think it does. Also, on the clinical side ratios aren’t used in assessing risk and or lipid goals. Why you didn’t consider LDL-C is worrying.
With all the unknown regarding this lipidology, I prefer to default to eating the way people ate before junk food and high carb diets became the norm. That would have been a high fat, low carb diet. Was heart disease a big factor in mortality stats at that time or not, or perhaps unknown . I will wait to see more definitive study results before trying a drug that has multiple side effects and questionable effectiveness
@@robertusga everyone has apob so using the word causal is not correct. Remnant Apob (apob-a) is the actual problem and is most closely associated with high triglycerides in the blood. That is why we both agree that low carb works because it lowers triglycerides. It is not true that non vegan diets raise apob in all people. Though in some a high fat diet may raise apob. Its not proven that high apob with little or no apob(a) is causal in cvd.
@@JD-rc6lq well you must know something Thomas Dayspring and all other lipid experts must have missed in their life long career on the topic. Please, enlighten them.
Lol, apoB , ldl , nmr...ldl....mmunicate..a p.o. b...... N mr . Thanks . Eyes mind heart and soul wide open no fear... mobile transfer . Ya got it ... N mr, a p.o. b.
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I can’t believe this sort of content is freely available on the internet (please don’t change that!). Thank you for putting these out there
Such a nice person tom is.. I am a physician and i Learned a lot from him.. My whole thinking has changed regarding lipoproteins and CV risk. Thanks peter for such great podcasts.
I've studied many scientific topics and came accross lipidology fairly recently, and I don't know why I've never been excited as much as I am about lipids... So for me it's no surprise your podcasts on lipids are a hit!
I'm not a physician, just a patient trying to understand my own lipids and risks. I was disappointed that in this entire interview, not one single mention was made of studying and changing the patient's dietary intake of macronutrients which are the inputs into the lipid metabolism. For example, if someone has extremely high triglycerides, instead of using a drug to lower that, shouldn't the first line of treatment involve altering the lipids and carbohydrates in the diet?
Because they want people to take statin? There are keto/LCHF diet that would effectively lower Triglycerides for most people, but might increase LDL (and APO-B) for some.
I think there just isn't one answer to that question. People respond differently to different approaches.. I lowered my TG from 170 to 53 in a couple months by switching to LCHF, but my LDL went up 40%. You don't know until you try.. tweak, analyze, assess, repeat.
yep.
My LDL-C went up too, when I did a LCHF diet pattern of eating. My doctor was concerned, but I wasn't because I had studied that LDL particles that are large don't cause atherosclerotic plaques. It's the small dense LDL particles that are atherogenic. My ratio of TG/LDL-C, which was 2.0 (in American units), indicated that nearly all of my LDL was not atherogenic. @@SwoleTown Watch A/Prof. Ken Sikaris - 'Making Sense of LDL' ruclips.net/video/2p-mkbNutvQ/видео.html and this link jumps to the part of another lecture where Dr. Mason explains how to tell if your LDL are large (pattern A) or small (pattern B) from standard lipids tests: ruclips.net/video/DXKJaQeteE0/видео.html .
Crazy timing. I finished the last 5 part series for the second time last night while falling asleep. I wake up and this is in my notifications.
Thank you Peter and Tom for giving so generously of your time to make these very detailed and inforrmative podcasts which instruct the world. They are so so helpful. I am very grateful.
Excellent podcast! Very helpful. I also really enjoyed #20-24 and this was a fantastic update. Thank you so my Dr. Attia and Dr. Dayspring!
Listening to Peter's vids have made me way more critical whenever I listen to other people discuss health and wellness.
More often, when watching other videos, I find myself saying, 'ehhhh, Peter Attia would likely stop you right there and have something to say' lol.
That's good though, because even if one doesn't fully understand a topic, it's good to at least know when to start being critical. Like when statistics or any kind of number are being cited
Had a cardio IQ panel from quest come back with phenomenal numbers in all categories from a standard lipid panel as well as apob and LP(a), but LDL-P was high risk. My question was how can apoB be low while the particles that contain apoB were high? Discordance among the "same" particles. Thank you for clarifying that NMR can be inaccurate for LDL-P and that apoB should be the metric for risk when discordance is seen between these metrics! What a headache trying to track this down haha
I just got really confused...you asked him about the effects on Lp(a) from statins and other drug and he started talking about ApoA...aren’t they two totally different things? I’m lost...
Yes
Dr. Attia,
Please consider: if arterial schelorosis is the result of an inflammatory response. As insulin resistance increases, increased glucose damages the arterial wall, allowing cholesterol to enter the arterial wall. Reduce insulin levels, reduce arterial plaque.
Am I headed in the right direction?
Excellent discussion on a complex topic
While I've enjoyed and been greatly informed by your podcasts, the lipid series are frankly confusing, scattered and poorly organized. This is especially true of this last one. I think it's confusing because lipidologists haven't figured out the mechanism for atherogenesis and therefore haven't really figured out what and how to measure. It would have been better organized into Rumsfeld's knowns, unknowns, known unknowns and unknown unknowns.
I’m not sure what you mean. The response to retention hypothesis is the mechanism for atherogenesis.
@@ucchi9829 I thank you for your remark as it led me to find supplementary resources: here is one from Dayspring and it's a very clear exposition in PPT form: ruclips.net/video/89QEoUaxiDo/видео.html&ab_channel=TrueHealthDiagnostics and is an oldie but goodie from Peter Attia re cholesterol: peterattiamd.com/the-straight-dope-on-cholesterol-part-iv/
@@gondwana6303 Attia's take #7 is wrong but I think there are better posts/reviews on this topic. I'll link you a video and current literature:
ruclips.net/video/wJKqq3ERLFs/видео.html
Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel academic.oup.com/eurheartj/article/41/24/2313/5735221#198921792
The Role of Lipids and Lipoproteins in Atherosclerosis
MacRae F Linton et al 2019 www.ncbi.nlm.nih.gov/books/NBK343489/#_NBK343489_pubdet_
Thank you for this podcast. I love the content.
Very informative. Thanks 🙏
What you recommend as an appropriate apo b level based on age? Is this a marker you expect to increase as one gets older?
My Lp(a) is always rock bottom low (3 nmol/L or 1.34 mg/dl) but even on a ketogenic diet long-term (15 years) I have to take niacin to lower my triglycerides.
LDL/TRIGLYCERIDES level sounds like a good test to do .... But where to go ? Any lab name?
If you have a PCP who orders routine blood tests for you, Trigs OUGHT to automatically be included along with HDL and LDL PARTICLE SIZE, Good luck-tit will really help to know those figures. 😋👍
Thanks a lot
39:27 If HDL isn't a significant factor in predicting disease, then is the TG/HDL ratio now mostly useless? And if useless, what data is most useful from an average cholesterol report.
The ratio is useful it's not as sophisticated and up-to-date dr.day Springs level understanding. What is most useful is Apo B. Apo B is part of LDL if LDL is not super high they both correlate. Also get a one-time test for Apo little a. It is pathological and not everybody has a pathological level of it.
I think it's very useful, and as he stated, it's the "why" that matters.. why are TG high and HDL low? probably because you're insulin resistant. That, then, can lead to dramatic increases in ApoB, slower clearance rates, increased chances of atherogenesis.
At the 23:05 mark, you mentioned that you have a patient at your practice with total cholesterol of 300 and LDL 220 APO B 170 but her CAC is zero. Did you check her soft plaques? Maybe there are many more exceptions like her? Maybe APO B is not such a good CVD indicator? What is her triglycerides to HDL ratio?
Wow, thank you for this talk, I've been so spooked by the statin boogeyman, this talk has really calmed the worries.
22:37 is he trying to talk about the response to retention hypothesis? Which doesn’t posit endothelial damage actually
First Responders must be bad, they're found at the scene of nearly all fatalities.
But when you're first responders are being forced to carry torches and gasoline, which they set down at every scene, they're also a problem.
Of course the answer is to stop the source of torches and gasoline, not to fire all first responders.
@@Unsensitive but that’s not necessarily the context which the blood lipid conversation, and specifically LDL, is being painted by the vast majority of those who still carry a torch for the old health heart hypothesis and ultimately the wide scale dispensary of statins.
I don't think that's what's being stated here, or in the entire 5 part series. In fact, it's stated multiple times that LDL isn't a great marker, and that ApoB should be used in it's place going forward.
@@wmartonejr apoB/LDL has been proven to be causative of cardiovascular disease through numerous different mechanisms of sample sizes of hundreds of thousands in prospective cohort studies, randomised controlled trials and Mendelian randomisation studies which all show the same thing. No one is basing it off mere association. It’s proven in the outcome data that lowering LDL causes massive reductions in all cause death.
So what do we need to do to live a healthy, energetic life . ???? REPEAT WHAT SHOULD WE DO ?? EYES MIND HEART AND SOUL WIDE OPEN NO FEAR....
Why would anyone follow the advice of a doctor who is 100 pounds overweight?
Sometimes people have the correct knowledge, but do not, for whatever reason, implement it well in their own life. It is easier to say what to do than to actually do it.
The content is more important than the messanger or the delivery, but most people have been taught to trust information based on the credentials, authority or delivery of the presenter.
@@edpomi or it means that his findings have no practical use and are of academic nature only.
@@wocket42 the fact that he is overweight has nothing to do with whether is information is of no use or academic in nature only. I don't think that all of his lipoprotein babbling is of any practical use, but the initial comment had to do with a logical fallacy of judging the nature of the content on the appearance of the presenter. That type of logic is why people think that the stuffed shirts of corporate media are authoritative.
I'll
23:31 how does a CAC score of zero mean that a lipid lowering therapy isn’t warranted?
Cac of zero means no hard calcification
@@museitup4741 and?
@@ucchi9829 CAC of zero is a strong indication that you are not at risk. Of course, it is not fool proof, but if you have good lipid profile (2:1 ratio of hdl/trig) and a zero CAC score, I personally would not touch a statin
@@museitup4741 no.
@@museitup4741 the literature on CAC scores is weak first of all. Second, on the clinical side, they are only considered in very specific scenarios.... if you fall into the low risk category and you’re around 40+ you can talk to your GP to see if it’s worth considering. A CAC score doesn’t reflect what you think it does. Also, on the clinical side ratios aren’t used in assessing risk and or lipid goals. Why you didn’t consider LDL-C is worrying.
36:04 they can also pass through via transcytosis
Option A low carb
Option B crazy drugs on a poorly understood system with unknown side effects
With all the unknown regarding this lipidology, I prefer to default to eating the way people ate before junk food and high carb diets became the norm. That would have been a high fat, low carb diet. Was heart disease a big factor in mortality stats at that time or not, or perhaps unknown . I will wait to see more definitive study results before trying a drug that has multiple side effects and questionable effectiveness
@@susantroupe9341 oh man. Your ignorance is really vibrant here.
Low carb animal based raises ApoB which is causal in CVD. Unless you mean plant based lchf then yes.
@@robertusga everyone has apob so using the word causal is not correct. Remnant Apob (apob-a) is the actual problem and is most closely associated with high triglycerides in the blood.
That is why we both agree that low carb works because it lowers triglycerides.
It is not true that non vegan diets raise apob in all people. Though in some a high fat diet may raise apob.
Its not proven that high apob with little or no apob(a) is causal in cvd.
@@JD-rc6lq well you must know something Thomas Dayspring and all other lipid experts must have missed in their life long career on the topic. Please, enlighten them.
Lol, apoB , ldl , nmr...ldl....mmunicate..a p.o. b...... N mr . Thanks . Eyes mind heart and soul wide open no fear... mobile transfer . Ya got it ... N mr, a p.o. b.
What you recommend as an appropriate apo b level based on age? Is this a marker you expect to increase as one gets older?