And of course one of the many things that Dave has done is predicted beforehand what he expects his level to do before his experiments and then reports back… I’ll go with that over some “theoretical” argument every time.
He’s in tune with himself. If he could predict what mine would do from a food log and a previous test, then he’d have something mintable.
Thanks for your perspective. That makes sense.
Attia and Dave come at it from slightly different angles. Attia treats patients every day and must give them recommendations based on best medical knowledge (implied w/o incurring malpractice liability). Dave is interested in chasing down a theory that is more of a system view rather than individual component view. His desire is to do big data multivariate analysis to determine the plausibility of his theory. So one guy is taking a engineering perspective and the other guy is based on medical experience and practices.
Not to get off on a tangent. One thing that really seem disingenuous of Attia was toward the end where he said that the keto community was only interested in confirmation bias. That does not describe me nor a lot of people I know here. I’m trying to address a predilection for T2DM any reasonable way possible. He also stated the keto community should be the source of funding for Dave’s research. Both of these statements really harmed my view of Attia. Many medical bodies accept tons of gov’t $ for research and big pharma and insurance companies fund much doctor education/research. Dave’s research requires small $, no liability and access to data. I think the medical community may be giving him a cold shoulder, denying him access to needed data. That would be confirmation bias…
it can’t be said any better.
Bret is a Dave fan - but also approaches his podcasts with thoughtful critique.
She’s a smart cookie for sure but I wouldn’t call her an expert in anything TBH. Her twitter is nothing but link dumping abstracts, most of them really shitty studies and her only defense for posting it is “I’m just posting it”. Barely weighs in on it. During that interview with Joe, she had nothing other than the untested argument to debate carnivore, so she resorted to using words like “putrefaction” to describe what happens to protein in the colon.
She didn’t account for the fact that meat protein is absorbed in the small intestine and very little even makes it to the colon, the studies showing putrefaction are based on PLANT PROTEINS (which she should be well-versed in, since she barely studies anything but plants it seems).
Half way through. Need to re-listen to it from the beginning again at least once before I have a considered opinion.
I agree. But I am willing to believe that a lot of smart people miss the wood for the trees, so I want to unpack the entire conversation.
Peter talks often about his bouts of severe depression, and has hinted at dark even suicidal moments. I feel sorry for people with this kind of AAAA personality because they often have trouble achieving self satisfaction in the quieter moments of their days. Me? I’ve don’t think I’ve ever had a problem feeling happy and content.
I do very much enjoy his precise use of language. I think he’d make an excellent university lecturer. I think he was wasted as a fund raiser for NuSi and as a private general practitioner working on high net worth individuals. I’m glad he appears to be getting his groove back with this podcast, although some of his subjects (like F1 racing) are not my cup of tea.
I think if I ever write an autobiography it’ll be titled “No drive”
You know there are weak associations between SFA intake and LDL-c. And there are weak associations between LDL-c and cardiovascular disease. Also there are over 16 studies that have tried and failed to find a link between saturated fat intake and cardiovascular disease, in fact many have found a benefit for example with strokes.
It’s non scientific to recommend someone reduce SFA to lower CVD risk. Clearly the population of people who see more LDL when they eat SFA are different from the population who have higher LDL-c and cardiovascular disease. Or the specific LDL particle raised by SFA are somehow different than the specific particles that are high in people who suffer cardiovascular disease. Or dietary saturated fat is more beneficial to reducing incidence of cardiovascular disease than any risk from raised LDL-c.
I’ve listened to several of his podcast. I like them very much, especially how he really lets the interviewee talk and he just gets right down to the nitty gritty. He doesn’t waste time bull…
Edit: couldn’t figure out how to smudge my naughty word.
I finally got through it.
Geez, I really wish Attia would have let Feldman finish his sentences more often. It was like listening to an overbearing parent who keeps correcting their children in public on why their opinion/hypothesis is incorrect, and why theirs is the only right way to think.
I need to reread the transcript now to see what I missed when I was irritated by Attia talking over Feldman.
This is exactly what I mean by Attia having cognitive dissonance, and why I stopped following him years ago. What does he do by citing the the “overwhelming” number of studies that support his theory? Confirmation bias. He accuses others of the exact some thing he does.
Compare Attia’s writings with the writings of Dr. Malcolm Kendrick: https://drmalcolmkendrick.org/
You’ll find that Dr. Kendrick is constantly trying to prove his theory wrong. You don’t get that with Attia.
The other problem I have with this whole area is that these studies are really epidemiological (epi) studies. We slam epi studies in nutrition all the time as proving correlation, not causation. But when we replace “saturated fat” from a “nutrition study” with “LDL-p” from a study on “heart disease”, suddenly they are sacrosanct. But they are still epi studies. Why is there no “these prove correlation only not causation”?
The final problem I have is that if you’ve the whole “cholesterol” theory for as long as I have, it continually morphs. You can’t kill it. High TC = bad. That doesn’t work? Ok, high LDL = bad and HDL = good. That doesn’t work? Let’s try many different ratios (I’ve even seen log ratios used). Those don’t work? Maybe it’s the new darling, LDL-p or whether your LDL is “fluffy” or “hard and dense”. Has it occurred to anyone (other than Malcolm Kendrick) that maybe these are just markers for something else that actually causes heart disease?
The fact that they could be does not cross and has never crossed Attia’s mind, and that’s why I stopped following him. I’ll check back once I finally get a chance to listen.
Bob, we’ve never met but you know me so well.
Please repost your thoughts when you have time. I’d love to have Dave’s post interview thoughts also. But I don’t think he’s here…
Agreed. Taubes talks about group confirmation bias as does Noakes. While it may not be bad intentions, overturning “existing bias” can be incredibly hard and professionally dangerous.
Agreed. Also, I was disappoint with the NuSci outcome teamed with Taubes. I had hoped they would be something like virtahealth. It was very interesting and a bit emotional to hear his Ted talk about his lack of compassion for a diabetic patient in the ER about to lose a foot. With more knowledge about how wrong conventional advice is for diabetics he felt bad about it. Could history be repeating itself with him not properly questioning the data on which his detailed knowledge resides? Secondly, much was spent on hyper responders. What about more normal individuals, much less the short term cholesterol numbers which run counter to conventional insight. I do not recall this being discussed.
I will relisten again as I have time. I would also like to hear Dave discuss what was resolved/learned from the interaction and how his perspective has altered. I think Dave’s intellectual honesty is outstanding. Lastly, I wish the gov’t would fund some counter research.
I listen to some of Peter’s podcasts because I want countervailing information. But I agree that he is focused on extreme topics and seems to forget that there are real people with deranged metabolism, T2D and more, with real hard jobs and modest money that have to overcome the SAD diet, Standards of Care and the ADA recommendations.
Dr. Mike Eades was on about this a decade ago. There have been LDL and Cholesterol skeptics for as long as there have been tests and medications for LDL.
If you look at the few studies that look at remnants, you see stronger relationships. If you look at chronic inflammation and insulin resistance, I suspect you can square all circles and resolve all paradoxes. As there really isn’t a drug to lower insulin resistance, or lower chronic inflammation, or clear remnants, the majority of studies will keep flogging LDL-C and LDL-P.
Taubes has talked about why I think this won’t happen. Basically, they’ve been flogging the diet-heart hypothesis since 1976, vegetable oils over animal fats since 1980, and excessive carb consumption for the same period. The Government can’t turn around and say, “Well, we’ve made a mistake, and we’re sorry we’ve given you all diabetes, heart disease, hooked you up with statins and BP medication, but accidents will happen.”
I am not sure I can demolish Peters logic just because he misbehaved.
I will continue to be open minded towards this topic from both sides of the argument.
As I see it both Peter and Dave agree on most things relating to cholesterol.
A point of contention that Peter somewhat relentlessly focused on is their differing views on the reason(s) for the very high LDL levels of hyper responders to a keto diet. Dave suggests it largely starts out as VLDL which also transports triglycerides and after delivery of triglycerides become LDL particles. This is a core element of Dave’s energy theory of cholesterol which he has been using to make bold apparently successful predictions about how Dave’s LDL will respond to diet over short time periods. Peter expresses in great detail multiple reasons why he doesn’t believe Dave’s theory can be the primary mechanism driving the LDL numbers in the patterns seen.
Peter pointed out additional tests of which Dave was unaware that can help quantify things like the rate of cholesterol synthesis. I expect Dave will continue collecting interesting data, gain new insights and refine, overhaul or replace his theory.
Of most interest to me is the question of whether high LDL is harmful. Dave like many of us here believe LDL is a highly flawed measure of risk and there are better indicators such as particle counts, remnant cholesterol, oxidized LDL, triglycerides to HDL ratio, etc. Peter’s view is LDL is for heart disease what oxygen is for fires. Without LDL there is no heart disease. Everything else being equal the more LDL there is the greater the risk of heart disease. These views are compatible they just differ in focus. LDL doesn’t go up or down in isolation and one must look at the complete picture to make a risk assessment. Peter acknowledges that LDL has beneficial aspects such as with respect to neurodegenerative diseases and one must balance the tradeoffs between heart disease risk and everything else.
Peter is concerned too many people going keto are ignoring high and rising LDL. His way of expressing it has rubbed some here the wrong way. I’m however swayed by the concern to revisit my high LDL. I’m very leery of statins but swapping in more extra virgin olive oil and avocado for some of the coconut oil and animal fats in my diet is an easy experiment.
This is why I’ll probably take a pass on the podcast. It sounds like Attia was really defensive and went out of his way to “rebut” Dave in a way that he has not done with any of his other guests.
Unfortunately I am still not swayed because Attia or anyone else has not provided a credible explanation for why high LDL, in the general population, is independently deleterious in the absence of the system going haywire. He gets hung up on minutia and genetic abnormalities.
As soon as someone can disprove Dave’s central tenant of lipid energy trafficking, I will take high LDL with concern.
The question that needs to be answered is, why does LDL increase on a fast?
I mean, you’re not consuming any saturated fat whatsoever, and SFA is the big lipid boogeyman on keto.
You’re not eating anything. And LDL skyrockets.
The behavior of fasting lipids bolsters Dave’s energy traffic theory, and shows Attia’s concern to be misplaced, unless he also thinks the fasting state is potentially atherogenic.