ApoB, LDL-C, Lp(a), and insulin as risk factors for cardiovascular disease [AMA 43 sneak peek]

Watch the full episode and view show notes here: bit.ly/3QBvV8R
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In this “Ask Me Anything” (AMA) episode, Peter answers questions related to the leading cause of death in both men and women-atherosclerotic cardiovascular disease (ASCVD). He highlights the most important risk factors for ASCVD, such as apoB, LDL, hyperinsulinemia, and Lp(a), and explains the mechanism by which they confer risk and how these factors are interrelated. Peter also dives deep into the data around apoB to try to answer the question of how much residual risk is conferred for ASCVD through metabolic dysfunction once you correct for apoB. He also looks at the data around lifetime risk reduction of ASCVD in the context of low apoB.
In this sneak peek, we discuss:
00:00 - Intro
00:08 - A racecar analogy for understanding atherosclerotic cardiovascular disease
09:15 - Defining and differentiating apoB and LDL-C
12:36 - The interrelated nature of insulin levels, apoB, triglycerides, and ASCVD parameters
18:17 - Another way that hyperinsulinemia plays a role in endothelial dysfunction
In the full episode, we also discuss:
-Why Peter uses the oral glucose tolerance test (OGTT) with all patients;
-Is there any evidence that hyperinsulinemia is an independent contributor to ASCVD?;
-Thinking through risk in the context of high-fat diets resulting in improved metabolic metrics but with an elevation of apoB/LDL-C;
-Thinking through risk in the context of low apoB but higher than normal triglyceride levels;
-The importance of lowering apoB for reducing ASCVD risk;
-Data on men and women with familial hypercholesterolemia that demonstrates the direct impact of high apoB and LDL-C on ASCVD risk;
-Importance of starting prevention early, calcium scores, and explaining causality;
-Defining Lp(a), its impact on ASCVD risk, and what you should know if you have high Lp(a);
-Lp(a) and ethnic differences in risk;
-Why someone with elevated Lp(a) should consider being more aggressive with apoB lowering strategies;
-Addressing the common feeling of hesitancy to taking a pharmacologic approach to lower ASCVD risk;
-Peter’s take on the 2022 Formula 1 season and thoughts on 2023; and
-More.
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About:
The Peter Attia Drive is a weekly, ultra-deep-dive podcast focusing on maximizing health, longevity, critical thinking…and a few other things. With over 45 million episodes downloaded, it features topics including fasting, ketosis, Alzheimer’s disease, cancer, mental health, and much more.
Peter is a physician focusing on the applied science of longevity. His practice deals extensively with nutritional interventions, exercise physiology, sleep physiology, emotional and mental health, and pharmacology to increase lifespan (delay the onset of chronic disease), while simultaneously improving healthspan (quality of life).
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[@zhilahaghbin4766]

HI Dr. Attia; highly appreciate your content, you explain the material on Lipids very well, thanks to your perfectionistic personality to really get it right and be able to explain to lay people. I have been listening to you to the determinant of not doing my own CME , I was wondering if you could turn some of your videos, podcast so that we could earn CME? I think that would really benefits all of us. thanks much for your passion and sharing your knowledge with us.

[@asarcadyn2414]

I think Peter hit the nail on the head when talking about endothelial dysfunction. Plaque, which is mostly calcium and scar tissue and not ApoB particles, 100% requires endothelial dysfunction to form. ApoB will naturally increase in the presence of endothelial dysfunction as it’s the job of lipoproeins to carry repair materials to sites of damaged cells. By trying to lower ApoB, you are putting the cart before the horse. The cells are already damaged and need to be repaired. You need to eliminate endothelial dysfunction. It makes no sense to lower ApoB with drugs when looked at from that perspective. Lower the inflammation that causes endothelial dysfunction.

[@JMK-vo8pv]

Couple questions- (1)Would you agree, Dr. Attia, that if a person has a PERFECTLY HEALTHY/INTACT coronary glycocalyx and endothelium, then the levels of LDL-C, LDL-P and ApoB particles are IRRELEVANT? (2) How do you explain that some elderly humans with very high Lp(a) levels have pristine, clean coronary arteries on invasive coronary angiography?

[@asarcadyn2414]

@@JMK-vo8pv I've been asking why the human body has evolved to kill itself for ages. Crickets.

[@JohnSlack89]

I have asked this question in an AMA on The Drive website as well. I haven't yet gotten a response, but I was able to look into the literature myself and from what I found, it does appear that there may be some mechanisms of too much apoB actually initiating the endothelium damage as well as being the carriers of the lipids that form the plaque. So in that way, excess blood glucose, homocysteine, chemicals from smoking, etc all have the ability to start that damage - only ApoB can both start it and continue it. So the horse may still be in front of the cart to do everything possible to lower ApoB if it does, indeed, initiate endothelium damage.

[@JMK-vo8pv]

@@JohnSlack89 That is a very interesting point, John. I will have to do some more investigating on the topic. However, I still find the ApoB "dogma" a little shaky since there are many people who have very high ApoB blood levels, especially high LDL and Lp(a) levels, and these folks have perfectly clean coronary arteries (NO PLAQUE WHATSOEVER) on their invasive coronary angiograms or their CCTA's. It really makes sense to me that the glycocalyx/endothelium get injured by many potential offenders (excess glucose, excess insulin, sickle cells, COVID19 virus, cigarette "nanoparticles", etc.) at the very beginning of the atherosclerosis process and then the apoB particles end up in plaque because they are trying to repair the inflamed coronary intima/subendothelial space.

[@JohnSlack89]

@@JMK-vo8pv where there is conflicting evidence, all I can look to is the evidence credibility pyramid - and anectodal evidence and single case studies are at the bottom while RCT's, meta analyses, and Cochrane reviews are at the top due to their large number of participants, critical reviews, and controls. And those most credible sources suggest that those with high ApoB are more likely to have clogged arteries. So while outliers will always exist for any number of genetic or environmental extenuating circumstances, there is nothing dogmatic at all about following where the majority of the evidence points.

[@cattleprods911]

Excellent chat, thank you gents!

[@bennguyen1313]

Regarding how some flavor of ApoC3 will not code for as many proteins, and thus more ApoB can be cleared... is there any benefit to checking your ApoC3 status?

[@alchemist585a]

When is the book coming out? If it's not too late be generous when it comes to diagrams, illustrations, & relevant biochemical pathways. Also, please use the phrase "energy factories" (to describe the mitochondria) more than once or twice. Thank you

[@videoagogo1]

Was it 'cold tyres', debris or steering column that caused Senna to fatally crash on a simple corner like Tamburello on Imola circuit?

[@dr.samierasadoonalhassani2669]

Thanks for naming the specifics .

[@rualablhor]

Keep your apoB low, exercise regularly, fast occasionally, and sleep well😉

[@gloriacavanagh1672]

Very interesting! Thankyou. Those light jokes are nice also!

[@michaelberman3648]

Because I thought that the particle size of the lipoprotein-C can be a strong predictor of a cardiovascular event. And I also thought that the number of very small or even small particles in relation to the total number of lipoprotein-C particles is a stronger prediction of early cardiovascular disease. My other question is: Does the particle size of a given lipoprotein-C predict the redox potential of the lipoprotein’s surface structure? And if the redox potential is greater, does that infer that the surface of this lipoprotein is more “sticky” or “stickier” to the membranes of the endothelial cells lining the inside of an artery? What I’m also asking, is the dipole -dipole attraction after oxidation occurs much stronger which allows that lipoprotein surface to become attracted to the endothelium more so or is it just the size of the particle that allows the lipoprotein-C to actually slip in between these epithelial cells???

[@juliebrown8375]

The cholesterol enters the endothelium by active transport. www.ncbi.nlm.nih.gov/pmc/articles/PMC7951609/ Particle size doesn't really matter.

[@elschumi]

I always had elevated LDL and ApoB levels but quite low LP(a) of 4mg/dl. I wonder if there are epigenetic differences that play into this as well.

[@ultimate8550]

I was about to post a comment with this exact question. My apoB is 125, but my LP(a) came back as

[@Hello-qs6me]

​@@ultimate8550wow! Exactly same here. Did a blood test and lp (a) was 8.4, but apo B stood at 125.. while LDL was sky high at 191.. really confused with so many contrasts

[@renatinhocunharc]

hello Peter , i an fron Brazil i born 76 big fan off Ayrton i an also orthodontist and have bean folowing some off yours advices...thanks somuch sharing such a good contents

[@HN-er2km]

Dr Attia. I live in sugar land , Texas. The family doctors so far I have seen so far did not seem to be very good in LPa and LDL treatment. Any specialized doctor do you recommend to check an treat my cholesterols?

[@mosesramirez6330]

Consider looking for a doctor who specializes in internal, functional, or holistic medicine or a D.O. These designations aren't a guarantee, but it's a good place to start narrowing down.

[@Gypsy218]

I think you’re both sometimes saying insulin when you mean glucose

[@sashafroyland]

The race car breaking before a cliff analogy is good.

[@derekheckley9447]

Can you do an episode about type 3 diabetes?

[@SupremeODMG]

Also not so worried as medicine if we are alive in the next 10 years should advance drastically, especially once A.i becomes more common. We should be making more discoveries and hopefully develop better treatments. The issue is if we don't have anything else cause us destruction first. I'm not worried about ApoB more than I am the world killing me in 10 years.

[@BigPictureYT]

Thanks.

[@alphacause]

To play devil's advocate, is there anything about ApoB that is beneficial or necessary, such that driving it down to ultra low levels could be harmful? Are we trading one benefit - better cardiac outcomes - for another harm, like increased cancer risk? I have no evidence supporting the idea, I am just wondering if anyone here has seen something like that. The reason why I bring up this possibility is because many times in the history of medicine, our attempt to drive something down or up in our bodies, which we thought would improve our survival outcomes, came with unintended, and often negative, consequences.

[@wocket42]

Yes, cancer, deadly infections, etc. Every time you block a natural homeostasis from happening, something bad will happen.

[@user-fl5lr1nm5v]

It depends. Anything in excess is harmful, including ApoB. A modest amount of food is good, an excess is bad, no matter how ‘nutritious’ the diet. Perhaps the production of ldl or apoB has gone awry for whatever reason (like a cancer).

[@juliebrown8375]

No. Every tissue in your body needs cholesterol, but fortunately all of those tissues make their own supply. You don't actually need any extra floating around in your blood stream.

[@user-fl5lr1nm5v]

@@juliebrown8375 Yes, every cell has the ability to make its own cholesterol. The question then becomes ‘why is cholesterol being manufactured in the liver if all our cells can make their own?’ Mother Nature has made a mistake or we just don’t know enough yet? Unfortunately it’s never as simple as we imagine 🙁.

[@fastridesports5225]

Would you be able to do a podcast on getting back to exercise after a heart attack? I had no warnings after regular check ups. I had a non stem I heart attack while mountain biking. I now have stents in my LAD and want to understand exactly how this effects my return to exercise. It was so unexpected within in my own community because I was known as the fit old guy. Any chance you could do one on that? PS , I’m a big RHCP fan 😅

[@29sigus]

I think you can go exercise with caution the same thing happens to me and I was very worried about going back to the gym by walking 30 minutes daily it will help you getting back to normal life don’t forget supplements

[@fastridesports5225]

@@29sigus Thank you, I appreciate it.

[@plants_and_wellness1574]

Have you tested your Lp(a)?!

[@fastridesports5225]

@@plants_and_wellness1574 no I haven’t.

[@plants_and_wellness1574]

@@fastridesports5225 if you’re one of the ones with genetically high Lp(a), that could explain your unexplained heart attack. I have high LP(a), so that’s why your comment got my attention.

[@mdh157]

there is some research indicating Niacin can lower lp(a) significantly.

[@cubalkan]

Also Vit C, Lysine and cysteine

[@k29lee]

Peter, can you address the correlation btw consumption of untiltered coffee and elevated ApoB or LDL-C? Do you recommend reducing intake of coffee crema? I reduced my LDL-C by 55 (169 to 114) after cutting my espresso completely for 2 months. Just did it myself, not at the direction of my PCP (she had no idea about the correlation so had to educate her).

[@Youssef-1911]

is that the only change u did ? and how many coffee u took per day ? cause all recommendation for black coffe is ok :( in my country there is no unfiltered coffe mostly we drink turkish coffee .. so dr say 2 -3 cup per day is ok

[@abejaamarilla4961]

That is anecdoctal, coffe is ok, not when combined with flavors

[@locybapsi174]

​@@abejaamarilla4961 It's not anectodal. Unfiltered coffee does raise cholesterol significantly. But not paper filtered coffee.

[@williamkelly7461]

So my triglycerides are well with normal range and my crp is well within normal but just had APO 1 and it was 145 high ,i don’t get it veggie diet 25 years. Why?77 years old feel great.

[@juliebrown8375]

Genetics.

[@christopherstewart9874]

OK, bring this down to layman's terms. If LDL is not a laboratory measurement, only LDL-C or LDL-P, when the lab reports LDL (which they do) is it LDL-C or LDL-P? And why has no doctor I've ever been to requested ApoB when they order a lipids panel?

[@tmemore]

So what if you have high HDL, Low triglycerides and high ApoB, LDL? What does this mean?

[@jeremydrake101]

My apob is 120. What do I do?

[@guntherxtent]

I’m 41 years old with history of cardiovascular disease on both sides of my family, and my ApoB is 69mg/DL. Should I be aiming to lower it?

[@Markus-fw4px]

He mentions a target of 30-35mg/dl in case of positive family history.

[@vicpdx]

What percent of endothelial layer cells vs. glycocalyx health help prevent ApoB from getting through.

[@arnoldfrackenmeyer8157]

What about environmental issues and ASCVD?

[@TheAuthenticityProject88]

My LPa, LDL & ApoB are high. My blood pressure, insulin & HDL are all good. My CAC score is 0. My EKG and echo cardiogram are both good. I workout 4-5x a week and I'm 35 years old. I'm adopted and recently found out both sides of my family have ppl who died from heart attacks... Awesome 👍 I'm pretty obsessively anxious, so I really research stuff like this bc I'm mostly scared to death im toast. I gotta say, the more places you read and listen, the more you realize ppl just say a ton of shit about this shit. Sometimes rly fit runners die at 40 with no signs. Sometimes ppl w CAC scores of a billion and family history who are overweight are A OK and in their late 70s. What's my point? The internet is killing me

[@azerko]

How cool is that you are using a senna shirt. Is it a senna helmet back there? Cheers from 🇧🇷

[@jamesficaro4332]

I’m 36 , I have high ldl and high total cholesterol for 10 years now but have a calcium score of zero , normal blood pressure , insulin is good and never smoked . The doctor wanted to put me on a statin which I thought was crazy . I would like ur 2 sense . Thanks

[@josephramone5805]

You're not going to get any amount of "sense" from these guys because you're not their target audience. They seek pharmatherapeutic sheep.

[@2005kpboy]

May I know how high your 'high' LDL and total cholesterol are ?

[@juliebrown8375]

CAC measures calcified plaque. Calcified plaque takes decades to develop and a positive CAC score at your age would be very, very unusual. It sounds like you may have a familial hyperlipidemia. At this point, if your diet isn't crazy, a lipid lowering medicine is probably your best bet.

[@AdRock]

When are you going to begin offering telemedicine? I can’t find a doctor to prescribe pharma when my 10 year risk is low.

[@erastvandoren]

Just go plant-based.

[@mikafoxx2717]

@@erastvandoren yeah, that wasn't remotely what they were asking for.

[@michaelberman3648]

Are you inferring that the number of particles of a lipoprotein-c is inversely proportional to the size of the average of these particles??? This relationship of particle size & the number of particles of a lipoprotein-P which also carries cholesterol was not exactly clear to me from your discussion here.

[@rualablhor]

Anyone here knows if acute exercise (right before a blood draw) raises serum fasting insulin level, (like blood glucose)? And if so, by how much?

[@Snapkrackpop]

I think the intensity matters. Like a moderately intense strength training session will raise liver ALT enzymes. And can possibly increase blood sugar and cortisol as well. I think if you always get your bloodwork done after a workout, the results are more accurate than if you go sometimes after a workout and sometimes after no workout.

[@rualablhor]

@@Snapkrackpop yes, a moderately intense work out definitely raises bg abit via cortisol, usually around 20pts in my experience. I haven't read (find) or heard much at all with insulin however...

[@IlIKRATOSIlI]

Why is no one talking about the Pauling Protocol. What are things outside of western med never even considered. More drugs... Lp(a) is NOT a static number.

[@sc4332]

When commencing trt my apoB stayed the same, 73, but my apoA (hdl), went down. Does this matter. One expert has suggested that testosterone decreases the need for hdl?

[@SupremeODMG]

Nope apoA is just total hdl. How much did it go down?

[@sc4332]

@@SupremeODMG maybe 30%, which is extremely common with trt. I don’t think we’re yet to know why.

[@vince1229]

Good potassium levels stop and reverse arterial and aortic calcification.

[@johnny7808]

In the upcoming hdl episode please address the research that controls for alcohol intake and yet still shows an increase to mortality with very elevated hdl. Commonly celebrated on social media are those with very high hdl with no alcohol intake, as they contend they are more cvd-bulletproof due to their very high hdl, whereas the research suggests the opposite.

[@erastvandoren]

LOL, he won't. It will endanger his sponsor relations.

[@AZ89231]

Increased HDL-c related to healthy lifestyle modifications can be a reflection of healthier lipid metabolism and insulin sensitivity (HDL-c is almost like a pseudomarker of LpL activity which if is increasing, may mean that you likely have low expression of ApoCIII on your ApoB containing lipoproteins and you’re more metabolically flexible.) It’s not a super informative marker alone but can give some clues into health. Whoever thinks they are CVD bulletproof from just having high HDL-c is an idiot but I wouldn’t say ‘the research suggests the opposite.’ There are plenty of epidemiology data that support higher HDL-c associated with lower ASCVD risk but there is a stronger association with lower HDL-c (and higher TG) with higher ASCVD risk

[@Primetime_dads]

I can’t believe he cut it off right at the part to where he was gonna tell Is how to see if we got bad or good insulin response. I needed to hear that part more then anything. Can someone tell Me what he said 😂

[@OverJam52]

Not sure I understood, is LDL-p or LDL-c the real risk factor. He only talks about the concentration of LDL, could be both.

[@ivanfoofoo]

Both are markers, but the particle is the strong one.

[@mindhunter09]

Hyperinsulinemia may cause endothelial dysfunction, but so do animal proteins and processed oils. That is important to note.

[@dilettanter]

Animal proteins too?

[@mindhunter09]

@@dilettanter Yes. Look into TMAO produced by ingesting animal proteins, and how it impacts the endothelium. Dr. Caldwell Esselstyn and others are very clear about this.

[@dilettanter]

Thanks for replying! I’ll check it out @@mindhunter09

[@philipmarx1819]

I like these discussions, but the Mellow is off the charts.

[@lisanewcombe168]

Has peter ever done an AMA on HRV?

[@rualablhor]

I don't recall...and I have listened for awhile fwiw

[@davidobrien590]

AMA #31. Guess you haven’t been paying attention. If you really don’t know something, probably best to remain silent.

[@rualablhor]

@@davidobrien590 my bad, I do recall that one...but it wasn't that good imo. Well...*I didn't learn much...

[@davidobrien590]

All I remember is: below 14.7 is bad and I’ve been below that a few times lately.

[@Straightdeal]

What no one eludes to is this: There is a test (NMR) that gives you LDL-P (good) and LDL-P (oxidized). ApoB is a total particle count including VLDL, but also the "good" LDL. So it is a measure which needs to have the the LDL-P (good) deducted!

[@ApoBeef]

Hmm, Attia has never mentioned this I don’t think

[@palimpsestransparent]

As far as I know, NMR only measures particle size and number, not oxidative state

[@juliebrown8375]

Particle size is an older hypothesis that isn't well supported by evidence. Here's a good ApoB explanation. www.ncbi.nlm.nih.gov/pmc/articles/PMC8540246/

[@biscuithammer]

I have the same shirt! :D

[@lwu101]

Haha like that you guys need out on F1 at the beginning before getting into the subjects. 😂

[@johnroberts5500]

Chili peppers 🔥🔥

[@beepbeepnj2658]

"Nonetheless, the apo(a) size distribution in centenarians did not entirely explain the high Lp(a) levels observed in this population. Factors other than apo(a) size, and which may be either genetic or environmental in nature, appear to contribute to the elevated plasma Lp(a) levels of our centenarian population. We conclude therefore that high plasma Lp(a) levels are compatible with longevity." 1998 article by J Thillet

[@plants_and_wellness1574]

I’m confused by this because there are multiple studies showing decreased life expectancy for those of us who have high Lp(a)

[@beepbeepnj2658]

@@plants_and_wellness1574 Your Lp(a) levels are in your genetics for a reason you should not worry about it unless your levels are really high like over 150 mg/dL or over 400 nmol/L.

[@plants_and_wellness1574]

@@beepbeepnj2658 my recent levels were 380 nmol/L. Now that I know what I know I am no longer concerned. No one in my family has lived past 71, grandpa had first heart attack at 55 and was dead at 63 (1978) , grandma had 3 strokes and died in a nursing home at 70 (1990). They had 7 kids and two remain. I had my moms Lp(a) tested and it was in the 130’s. She eats differently from the rest of the family, no red meat. No saturated fat and her sister is the same. All the rest of them died with clogged arteries. My mom and her sister have never had heart problems and my mom has always refused a statin, not sure about her sister. Before I gave up red meat and raw milk my LDL was 194, my small particles were in the 1800’s, should be under 1000, now they are less than 1300, my LDL is now 112. I’m not going to worry about it but I am going to do everything I can to keep my ApoB and LDL particles down, the small atherogenic kind. Oh and my mom has smoked a pack of cigarettes a day for 55 years, her sister, too. Apparently own genes don’t mind smoking but stay the hell away from red meat lol.

[@beepbeepnj2658]

@@plants_and_wellness1574 It sounds like the type of foods caused the problems not the Lp(a), maybe it wasn't the meat but stuff like fried foods, fast foods, trans fats in donuts and all the foods that were invented in the last 100 years?

[@plants_and_wellness1574]

@@beepbeepnj2658 not much fast food back in the 70’s and they were really poor so they never ate out. My mom said they ate red meat regularly, and always had a big block of butter in their fridge. Those foods raise LDL-C/P as well as ApoB and small LDL particles which are very atherogenic. I feel like soon we will all be hearing about LDL-P and small LDL and how bad it is. My LDL-P was over 1800, a number that would shock most cardiologist and I was eating mostly plants but I had my smoothie with raw milk, I loved raw milk, and I had steak 1-2 times a week with organic veggies on the side, ground beef other nights or chicken, always with veggies covered in homemade butter. Since giving all of that up my LDL-P and LDL-small has decreased substantially and my Lp-PLA2 went from being elevated to being in a normal range. That is also an independent risk factor for heart disease and mine was over 200, should be under 123. Giving up animal products has helped me turn more than 20 cardiovascular markers around for the better.

[@AZ89231]

Revisit with Dave Feldman - need another episode with him. I’m afraid Dayspring wouldn’t allow it but Peter’s tougher than that.

[@robertusga]

Why? You need to give Feldman a bit more time to finegal study design some more and exclude more data he doesn't like from his LMHR study so he can make it work. Patience. Give the man some space already.

[@AZ89231]

@@robertusgalol think what you want. History won’t be in your side.

[@robertusga]

@adudz1 sure, keep the faith!

[@AZ89231]

@@robertusga don’t need faith, just evidence 😉 science is litigated empirically. We’ll let the numbers speak for themselves.

[@robertusga]

@adudz1 then you must already be blown away by outcome based data from RCTs, epidemiological studies and Mendelian randomization studies ALL pointing in the same direction: high ApoB is causal in CVD, which does not exist in folks born with life long ApoB in the 20s and 30s. All Feldman has is mechanistic speculation with 0 outcome data from a rigged study. You call that science?

[@considerthis7712]

The analogy of the car driving towards a cliff , says we will all die of heart disease, if something else does not get us first. 🤕

[@michaelberman3648]

Logically, at least one can declare that everyone’s heart does stop beating no matter how you die. But I would also think that many that do die is not necessarily due to any progression of cardiovascular disease but other physiological factors can also cause the heart to stop beating due to a lack of oxygen due to say a tumor gradually pressing upon a major artery or major vein or a similar situation caused by other complications or factors I would think.

[@triatct]

What about high LP(a) (148) High CAC (350) and normal APOB (88) HDL (95) TRIglycerides 50. These lower numbers have come from KETO diet. I don't want drugs.

[@mdh157]

how long have you been keto before these numbers were taken?

[@triatct]

@@mdh157 2 years or so

[@videoagogo1]

Research to confirm if a gram or two of B3-Nicotinic Acid may reduce your Lp(a) by ~ 35%

[@Eplemos4Life]

Can LDL be high if you dont eat saturated fat?

[@dr.proteomix1257]

Yes, in fact the most common cause of elevated LDL is genetic, not from the consumption of saturated fats.

[@erastvandoren]

@@dr.proteomix1257 Familial hypercholesterolemia has a prevalence of about 1%. So not, it isn't the most common thing.

[@erastvandoren]

Everyone eats saturated fat. The question is how much.

[@moa3821]

genetics, amount if sat fat, other lifestyle behaviours

[@wocket42]

Eating almost 100% saturated fat can lower your LDL. E.g. through phytoestrogens in coconut oil. Ergo: saturated fat isn't the culprit and eating phytoestrogens is probably as unhealthy as low LDL-C levels.

[@beepbeepnj2658]

ApoB is sort of the flavor of the month. If your LDL goes up then the ApoB also goes up, usually one follows the other and if LDL goes down then most of the time the ApoB goes down, same with ApoA, if that goes up then the HDL goes up, it's just to sell more tests.

[@nancyevans5176]

You can have excellent LDL, and your APO B can be through the roof. Go listen to Tom Daysring, Md.

[@beepbeepnj2658]

@@nancyevans5176 And what do you consider excellent LDL? And if you think Tom Dayspring knows anything ask him to explain this: "Remarkably, one-quarter of the centenarians had high Lp(a) serum levels even though they never suffered from atherosclerosis-related diseases." 1998 G. Baggio.

[@ApoBeef]

@@beepbeepnj2658 Doesn’t that mean that three-quarters of centenarians don’t have high Lp(a) serum levels?

[@beepbeepnj2658]

@@ApoBeef And some people with low Lp(a) levels can also be a problem. "The Lp(a) levels were inversely correlated with the CIMT in this population, suggesting that subjects with a low Lp(a) level may have a predisposition to carotid atherosclerosis. This finding was preliminary and should be investigated further in larger studies and in additional settings." 2012 article title, CIMT thickness in asymptomatic subjects with low Lipoprotein(a) levels.

[@nancyevans5176]

@@beepbeepnj2658 watch The Proof. With T. Dayspring. A treasure trove of good info.

[@phantomopera5525]

In true GenX fashion, rocking that RHCP T-shirt!

[@jaspalchanna4025]

Peter I hate these videos. Big fan but there's a bunch of waffle. I would LOVE getting straight into a topic rather than dancing around it for 10-20 minutes and then putting the good stuff behind a paywall. Just my opinion

[@mabelheinzle2275]

Thanks but sadly too complex

[@Rachel_2112]

Ayrton senna🇧🇷🇧🇷🇧🇷🇧🇷😍

[@catcan221]

Formula 1 ❤️❤️❤️

[@rashie]

👍👍

[@BurtSaun]

I liked Peter before, but him wear a Chili Peppers shirt has really made me a fan. They are the Beatles of the last 40 years.

[@shaleel]

I'm chilling at like 108 apoB. High cholesterol runs in my family, no other risk factors. I'm going to run a 2 week experiment where I do it all - fully vegan, zone 2 cardio 5x a week and see what happens. Assuming I can't drop apob to 90ish, I will just grab some statins

[@bigbobabc123]

I had the same problem. Nothing worked other then medication.

[@rualablhor]

Imo you should check the other biometrics before going the statin route. ApoB in itself isn't vital, and imo 108 is NOT dangerously high...mine is higher! And I do consider myself a relatively healthy person.

[@shaleel]

@@rualablhor its not that high, but I'm 29. Keeping it at 108 for the next 30 years is less than ideal. But I agree that its not a huge deal, I am just trying to have a heart attack at 75 instead of 65 if possible.

[@GianniVitucci]

@@bigbobabc123 I agree with Tak Lee below- I would take a deeper dive into perhaps VLDL or CAC score etc before the statin route. Getting LDL down (by use of statings) in itself has not been proven to be beneficial for outcomes. In my own experience, after starting (and high dose) of statins, my AIC started creeping towards pre diab and my ALT went through the roof. Both coming down now since off the statins.

[@rualablhor]

@@shaleel I don't know you and how healthy (or unhealthy) you are, firstly. I was simply stating apoB itself shouldn't be the only metric you should go on. You should add up your other biometrics into consideration eg. Hdl, ldl, triglycerides, LPa, ApoB, ApoA ratios, blood pressure, blood glucose, body fat% etc... It's unhelpful to say your Chlesterol is high, how high exactly? Secondly, your apoB could go up, stay, * or go down fyi. And veganism could be either healthy or unhealthy btw...

[@TheIgnacio777]

10 minutes into it, nothing said....

[@chuaskh]

He almost never gave any answer on how body reach that level and how to reverse it.

[@MsQ275]

wow, we must have listened to completely different videos bc he says a TON of informative content in the first 10 minutes. you may not have the cognitive ability to comprehend it though? 😢

[@Josh-Jones]

You poor weak thing

[@robbo03]

Do you not have a brain?

[@f-authority6926]

Attia is quite the business man. EVERYTHING that is free on youtube is edited to make sure that he doesn't tell people any specifics as to what they can do to help themselves. No detail on the drug interventions he alludes to or dosage. As far as DOCTOR Peter Attia is concerned, you only get to live if you can afford to pay his subscription fee! 🤔

[@bartrobinson2103]

Shady indeed

[@tatsumakisempyukaku]

He could just stop doing these videos to make the money he’s losing. He’s obviously dedicating time to do these videos, time that could he spent making him money as the doctor he is. Also, we can take the knowledge from these videos ask our own respective doctors about our concerns.

[@f-authority6926]

@@tatsumakisempyukaku You're missing the point. These teaser youtube videos are his marketing- both for his high priced MD consults and to sell his podcast. That's it. He's careful not to divulge anything without getting paid.

[@ApoBeef]

What do you mean? Idk about YT but on his Spotify he goes over which statins/ezetimibe/pcsk9 inhibitors he prescribes, what apoB levels he shoots for, how much rapamycin he is taking etc.

[@videoagogo1]

Attia's idea of a Frat party road trip is .. a weekend to Omaha Nebraska to attend a Berkshire Hathaway AGM lol

[@user-ml8lr5yw6y]

Lot of chemical terms all mumbo jumbo for the one who wants to know the real key things that are important for understanding ATCVD. 20 minutes and what is the real takeaway🥵??

[@videoagogo1]

low dose statin + PCSK9 inhibitor FTW 🤨

[@creativesource3514]

Don't educate oneself from KZbin about health and certainly don't listen to anything in the KZbin comments.

[@MsClarasophie]

You lost me completely with that childish Ferrari metaphor, please, just talk straight

[@JD-rc6lq]

SB Dugani JAMA "Association of Lipid, Inflammatory, and Metabolic Biomarkers With Age at Onset for Incident Coronary Heart Disease in Women" Better off spending time digesting that paper than this guys obsession with "obliterating" Apob...not sure how you will have functional metabolism after that.

[@claudiovecchiatto3260]

What's Peter drinking?

[@ES-qe1nh]

Probably Topo chico

[@danielmccarthyy]

Why are we talking about bullcrap “risk factors” rather than root cause??

[@loganjames960]

Its a combination of factors that can lead to cvd not just one root cause.

[@BurtSaun]

Let me guess, you are an acolyte of a certain diet or listen to a lot of chiropractor videos?

[@danielmccarthyy]

@@BurtSaun I understand that people like to shelve their intellect (if they have any) and let someone else do their thinking for them. Good thing you found Attia to do your thinking! Now take your statins and be quiet.

[@BurtSaun]

@@danielmccarthyy since you are clearly more enlightened, what is the root cause of ASCVD?

[@asarcadyn2414]

@@BurtSaun Inflammation? Why would plaque spontaneously form in healthy arteries?

[@user-ml8lr5yw6y]

Just a lot of irrelevant information and waste of time and no real message that is relevant. Both speakers are in the dark😎

[@knockstarstv5711]

Why do you talk so softly speak up bud!