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Oct 08

Guesting on the Peter Attia Drive (5 of 5) – Comments and Featured Thoughts

This final posting in the series is devoted entirely to discussion in the comments on the podcast. Share your opinions in the comments down below on anything and everything about this podcast from your perspective.

I’ll be featuring a number of these comments in this space as well. The likelihood of your comment being featured  doesn’t need to align to any particular position, but I do ask that it be respectful and without ad hominem toward anyone in or outside this podcast. (Attack ideas, not people)

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vernon
Guest
vernon

Great Job Dave. Some questions: 1: Why do you think Dr. Attia is skeptical of the CIMT and CAC? I could understand that there is some art to reading the images and variability due to that. But he seemed quite skeptical of them. 2) I don’t understand his adamant stance on how the studies on statins are conclusive on the benefit they provide. I think you might have touched on the issue when commenting on the quality of research. The studies have shown, I believe, that the reduced risk of cardiac events is on the order of 1% (probably wrong on the magnitude here), not even considering ACM. I think he stated that because the intervention was applied over such a short timeframe that the effect was very powerful. Thanks, Vernon

Joe Kalb
Guest

I love that Feldman and Attia had the mutual respect for one another to openly dialogue and disagree with another in longform format and that we get to listen in.

I know little to nothing about biochemistry. My perspective comes heavily shaped from the work of Weston A. Price and also, admittedly, from the low-carb “echo chamber.” That being said, my default perspective is that, in most circumstances, pharmaceutical interventions are more likely to harm than help.

I think Attia’s strongest point throughout the podcast is that familial hypercholesterolemia is phenotypic rather than genotypic, that it does not necessarily indicate that there is endothelial dysfunction, and therefore FH results should be considered when looking at how a LMHR (low triglycerides, high HDL, high LDL) might fare in regards to cardiovascular health. I know next to nothing about FH, so I would like to hear this dialogued more.

I do follow nutrition from a low-carb echo chamber, so maybe this just speaks to my bias, but I was surprised to see Attia so quickly shoot down any idea of using Triglceride:HDL ratio as an indication of metabolic health. I’ve never read that it is a perfect indication of metabolic health, but most sources I’ve read seem to think it is as decent of a proxy as you can get from a standard lipid screening.

I think Dave has mentioned something to this effect before, but I do find it telling that Attia would not commit to believing that a low-trigyceride, high-HDL, high-LDL group would have high cardiovascular risk.

I was very surprised at Attia’s reluctance to entertain all-cause mortality as a valid endpoint. I certainly respect his point that it would not be as cost-effective to track, and that a given factor (ex: LDL) could meaningfully affect a single system (such as the cardiovasvular system). However, I think Dave’s point is strong here. ACM is what matters.

I was very disappointed in some of the condescension Attia conveyed. It was disappointing not just for the condescension itself, but because it left a couple interesting conversation topics relatively untouched:

Untouched Topic 1: the available data sets showing low-triglyceride, high-HDL, high-LDL subsets without increased cardiovascular risk. Attia treated Feldman like he had only anecdotal data, but when Dave tried to bring up Framingham and stratification of large data sets by low-trig/high-HDL groups, Attia just asserted that HDL-C isn’t relevant and that Dave needs to talk to more lipidologists. (That exchange did follow a theme of Attia using lots of appeals to authority and vague references to “50 years of lipid literature”). I want to know what Attia thinks of that Framingham data.

Untouched Topic 2: Dave’s CIMT experiment. Attia likely would have called out two things: that it was anecdotal, and that CIMT is not that reliable of an indicator of risk. However, I find it to be fascinating: Dave’s CIMT improved and improved on keto until a Standard American Diet intervention worsened it, and the CIMT worsening corresponded with significantly decreased LDL-C and LDL-P. Truly, how would Attia think about Feldman’s cardiovascular risk with {SAD, increased CIMT, decreased LDL} vs. {keto, decreased CIMT, increased LDL}?

Attia argues passionately his viewpoint that LDL being harmful to cardiovascular health is now the default hypothesis. He uncustomarily loses his cool (and uses the negative epithet “LDL denier”) at the very idea of the burden of proof resting on the side of lipid-lowering proponents. Maybe I’m just too deep in the anti-medication low-carb bubble, but from what I’ve read, that strikes me as backwards. It seems to me that the burden of proof would lie with the side recommending the statin intervention.

Attia does indicate that there could be benefits to high LDL, just not to cardiovascular health, which I did find interesting.

There is so much biochemistry detail and so much knowledge shared between Attia and Feldman that as an untrained listener, I feel unworthy of even inserting an opinion. But this is the Internet, so what the heck: I’m not convinced by Attia’s view. I am intrigued to hear more of the conversation as to why FH data should or should not be considered as relevant to the LMHR CVD risk profile. However, as someone highly persuaded by the ideas of complex systems and natural remedies, I lean way more towards Dave’s viewpoint. I find it less than compelling that someone coming in, eating LCHF, who feels better than they’ve ever felt, should feel motivated to make changes to their diet or lifestyle to specifically target their high LDL-C and/or LDL-P (with other markers good). Of course, that is easy for me to say without my own skin in the game. But as an outsider looking in, in the context of low triglycerides and high HDL, I do not think I would be fearful of high LDL.

Stray thoughts on the podcast, Attia, and Feldman:

Attia is not as convinced about PUFAs being bad as he used to be. I’m curious as to why. I am strongly suspicious of PUFAs being the primary driver of chronic disease, so without further context, Attia downplaying their harm makes me a little bit skeptical of him.

I very much respect Attia’s point that this is not some idle intellectual exercise for him; he has real patients with high LDL that he must treat and counsel based on the information he has in front of him. That is clearly not something he takes lightly, which is very honorable. His patients are lucky to have a doctor so thoughtful and intelligent.

Dave’s understanding of cholesterol is generally not just explanatory, but predictive. That makes me think, though I have little understanding of the biochemical underpinnings, that his model is fairly robust. I love that in the July-recorded podcast he mentioned his hypothesis of how resistance training would lower LDL, and his September experiment confirmed it. He is also actively and genuinely seeking out data to disprove his theory, which speaks to his intellectual curiosity and honesty. Finally, Dave treats opposing arguments very charitably, which I think is admirable and deserving of more reciprocation.

All of that being said, thank you Dave, and thank you, Dr. Attia. This was a great listen.

Jamie
Guest
Jamie

I have so much respect for Dr. Attia and Dave because I believe they’re truly following the science rather than trying to prop up one view that benefits them financially. That said, I too got the sense that Dr. Attia was speaking down to Dave rather than as a peer. It’s interesting to hear that someone else did too.

There were times that I felt like they were dialoging as peers who were genuinely interested in exploring the other’s point of view. But there were some times where it felt like Dr. Attia was shutting that down because he just wasn’t interested in the idea.

This really caught me off guard as I have listened to Dr. Attia many times in other podcasts as well as The Drive (which I love). I’ve never heard him come across that way. I think it struck me so because it sounded a lot like the way doctors have talked to me as a patient.

I truly hope I’m misreading. I can certainly see the possibility that both he and Dave simply got caught up in the conversation and Dr. Attia’s enthusiasm came across as authoritarian because we were unable to read the body language. I will listen a few more times before forming a conclusion.

Shaza
Guest
Shaza

JOe, DITTO, your summary is wonderful…

jgilberAZ
Guest

Maybe I’m missing it, but I’m not hearing a lot of discussion about the effect of high blood sugar oxidizing LDL, making it atherogenic. I think it was touched on in the podcast, but not nearly to the degree that I think it’s relevant.

I’ve expressed my thoughts on apoe4.info (I am apoe3/4).
https://www.apoe4.info/forums/viewtopic.php?f=4&t=5212#p58643

I firmly believe that whether high LDL is detrimental or beneficial depends completely on whether or not it is exposed to high glucose.

For me, with Apoe3/4 and on a very low carb (almost carnivore) diet, I see my higher LDL as protective against all-cause mortality.

I just think the discussion about high LDL versus low LDL is rather pointless unless the discussion centers on the environment in which that LDL lives. Surely, it would be beneficial to reduce LDL if people are going to continue to eat carbs like they’re going out of style. But, if people ate a healthier diet, one in which blood sugar was kept low and stable, the efforts to reduce LDL would be counterproductive … all-cause mortality would increase.

Like the ambulance analogy … it’s not necessarily the number of ambulances, but the weather conditions in which they are operating.

Given that I’m literally basing my life on this understanding, it would sure be great to hear a thorough discussion of it.

BobM
Guest
BobM

I don’t want to derail this conversation, but your theory about high glucose may not be correct. Check out this post by Dr. Kendrick:

https://drmalcolmkendrick.org/2018/09/23/what-causes-heart-disease-part-56-a-new-paper/

I recommend reading all of his other 55 posts on the subject. In Dr. Kendrick’s view, LDL is a player (bystander?) but not a major one. Glucose may also play a role, again, not a major one.

Is Dr. Kendrick’s theory correct? It’s the only one that makes sense to me. Then again, the whole “fiber you eat reduces cancer” theory still makes sense to me…but it’s most likely wrong based on RCTs.

SPSalerno
Guest
SPSalerno

Join the discussion…It is just me, or did I not see very much discussion of insulin resistance as a key driver for CVD no matter what level LDL-C/P may be? IIRC, the MESA data was used to support results showing LDL-P as a more accurate predictor of CVD than LDL-C, regardless of particle size (Ovtos, et al). I would like to see if data was stratified by IR (or a surrogate like TRIG/HDL ratio) as well as by HDL, TRIG, LCL-C/P. Why do I think it will look a lot like the Framingham results? Maybe even better if those with high(ish) IR are excluded?

Dayspring, who uses the results of the MESA trial to guide his practice also provided information for Attia’s series on cholesterol, so I was more than a little surprised Attia was at a loss to know how to get the data. How about asking Jim Otvos??

I am also a lot more interested in ACM than other endpoints. If I’m going to chance side effects, I would at least like to know I’m going to live longer – a lot longer. That is hardly a criterion that leads to using a statin. The result of medicating LDL-P as per Attia/Dayspring is that if your LDL is anywhere over 150, you’re going to be on no fewer than two cholesterol lowering medications because a statin alone will most likely not be enough.

Jamie
Guest
Jamie

I’m only about half way through the podcast so far, but I’m left wondering what a LMHR should do. If they follow the SAD, they’re certainly on a path to diabetes and related issues. If they go the LCHF route and you follow Dr. Attia’s view, they’re also in a pickle. Does this suggest that the only path for a LMHR to extend quality of life is medication?

I refuse to accept that the body cannot function properly without pharma intervention. There must be some additional nutrition tweaking that can help. Perhaps a leaner form of low carb?

I am not a LMHR, but I’m still interested in this puzzle.

Jamie
Guest
Jamie

Okay, let’s fund Dave’s NLA meeting. How much do you need to raise for this Dave? Assume $1000 is just the registration fee.

Richard Arnesen
Guest
Richard Arnesen

Yes – I will help fund this!

Siobhan Huggins
Admin

Keep an eye out for an upcoming blog post 🙂

Yoav
Guest
Yoav

I know and agree we shouldn’t attack people, only ideas.
That being said, I do not like being overly politically correct to the point where I cannot say what my opinion is – I should be able to safely comment and share my thoughts on the attitudes of the interviewer and the interviewee without it constituting an attack.

After listening to almost 3 hours of what I assumed would be an informative and constructive podcast, what I can mostly say is that I am disappointed.

I appreciate and follow both Dr. Attia’s and Dave’s work, and continuously learning more and more.
But it seemed that instead of opening up and exploring new ideas (Dave’s per-se), this was more of an LDL-based argument. What’s worse was that both sides are aiming for completely different targets IMO and therefore seem to be having a shootout instead of a discussion –
Dave was aiming for modeling and understanding, while Dr. Attia was aiming at the practical, day to day clinical value of such and such (which as far as I am concerned is not relevant grounds for discrediting new ideas, especially when they may go against the grain and “established” knowledge)

Isn’t arguing about the level of LDL while disregarding all other parameters kind of moot?
Isn’t much of the data in the mentioned studies completely not controlling for diet (specifically LCHF vs HCLF)?
AFAICT this should be a critical point.
If my BP has dropped on a low carb diet and my LDL has risen, who is to say where the total benefit or risk lies?
If I take Ivor Cummins’ statistics as basis, then my data probably shows I’m better off on low carb, risk-wise.

Another thing was the focus on LMHR.
That is fascinating of course, but its only just part of a much broader picture which includes many people on low carb who are not LMHR.

Another point that seemed missing to me was the oxidation and particle lifetime as determinants on the effects of LDL on atherosclerosis. Isn’t that Ivor’s main issue and point about the whole LDL level argument being irrelevant (or at least very different) for LCHF?

As a last point I would like to commend Dave’s conduct. You seem very passionate about everything you do, but never let it become emotional. On the contrary.
As for Dr. Attia’s conduct in this podcast, I feel it was too emotional, and focused on “defending” current scientific knowledge instead of testing out new avenues such as the one Dave is suggesting – regardless of what the underlying truth actually is.
It was disappointing that Dave was treated as a doctor with patients (and was referred to as such by Attia!) and asked to answer for his positions regarding his “patients”, whereas clearly that is not the case nor Dave’s motive on this path.
I am personally following this topic to gain as much insight into the workings of the body. Not for clinical advice (which would be a nice bonus, but I know better than that).

Shaza
Guest
Shaza

I found it odd that Attia said Low Carbers used ad hominem attacks and within seconds he launched an ad hominem attack on Low Carbers calling calling them LDL Deniers! Dear Lord! Let’s stick to the science not the dogma, would be my main criticism of Attia’s whole style. Shakespeare: “The lady doth protest too much, me thinks”

Jim Ingram
Guest
Jim Ingram

I was beyond excited to hear that this podcast was planned. I was pleased that Dave was gracious and patient as always but quite frankly very surprised to hear Peter dominate the conversation and talk down to both Dave and also the entire Low Carb community. I originally got into the Low Carb Community reading Attia’s blogs on Cholesterol and Ketosis and viewing his YouTube presentation that made him famous. Those presentations and his other podcasts were universally very thoughtful, insightful, nuanced and productive. This entire podcast was not. Peter is clearly annoyed with unnamed members of the low carb community but his apparent disdain for the many other members of the community with sincere questions regarding these rare lipid abnormalities is disappointing.

Personally I am clearly a LMHR. I have lost 25 pounds, achieved 10% Body fat, am more fit than I have been in 30 years, and have 0 CAC, Normal CIMT, low Insulin, controlled BP, and all other screening tests normal that can be ordered. The idea that I would take a statin with an NNT of 120 – 220 with a NNH for diabetes of 60ish, myalgias 10, and decreased ACM due to increased deaths from cancer with PCSK9’s, is confusing. With such little power to lower my cardiovascular risk and such better health by all other measures, I’m happy to continue my current personal practices.

vernon
Guest
vernon

Repost because I think I posted in the wrong comment thread. If not then please ignore.

Great Job Dave. Some questions: 1: Why do you think Dr. Attia is skeptical of the CIMT and CAC? I could understand that there is some art to reading the images and variability due to that. But he seemed quite skeptical of them. 2) I don’t understand his adamant stance on how the studies on statins are conclusive on the benefit they provide. I think you might have touched on the issue when commenting on the quality of research. The studies have shown, I believe, that the reduced risk of cardiac events is on the order of 1% (probably wrong on the magnitude here), not even considering ACM. I think he stated that because the intervention was applied over such a short timeframe that the effect was very powerful. Thanks, Vernon

S.T.
Guest
S.T.

That was a very juvenile performance from Peter Attia.
If one asks a question , be polite enough to listen to the answer before cutting across with your own bias. Yes the facts are important, but until the facts are truly known, let’s respect each other. If you resort to argumentum ad hominem, you are the loser.

Guesting on the Peter Attia Drive (4 of 5) – Energy Status, Risk, Testing the Hypothesis » Cholesterol Code
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