Thread by @DaveKeto

1/Incredible exchange with @PeterAttiaMD and @ChrisMasterjohn! This latest episode is highly relevant to the podcast @PeterAttiaMD and I had last year re #LipidEnergyModel
----> It starts at 1:03:24 here: peterattiamd.com/chrismasterjoh… (All emphasis in this transcript image mine.)

2/ Attia: "This is a problem of flux.. Because you can’t understand flux with a snapshot, you have to have the goddamn video. I mean, that’s the analogy, I mean you take a picture of something and you don’t know the flux. What’s in, what’s out, where it’s being disposed of." Yes!

3/ @ChrisMasterjohn’s gives a great car accident analogy and explains how looking at only one piece in isolation is so probematic, “But if you’re looking at one element in the snapshot you can never even so much as build a story about what probably happened.”

4/ @ChrisMasterjohn: “And I think that yeah the idea that mistaking a concentration for flux is one of the overwhelming interpretive problems in science, and in popular science, in both.”

5/ @PeterAttiaMD :"...when I do one of these seven day fasts I get a lot of blood work done on myself... and I get a real kick out of it because by the time you're 5, 6, 7 days into water-only you start to look like there are things that if looked at in isolation look horrible"

6/ @PeterAttia: “For example, your free fatty acids get into a diabetic range. So if you show that to somebody they think “Oh my god you're diabetic” and you’re like, “Really?…”

7/ @PeterAttia: “My insulin is unmeasurable, my glucose is 60 mg/dL, yes my FFA is 2 mmol/L but my BHB is you know 7 or 5 mmol/L isn't it possible that what you're seeing is an incredible turnover of lipolysis?”

8/ @PeterAttia: “And so yeah there's a lot of free fatty acid there but it's in motion. It's in transit” versus what I think is probably happening in the person with high FFAs who's got diabetes…”

9/ @PeterAttia: “…which is a much more stagnant form of elevated FFA and so that's a muscle that's full of fat that's going nowhere vs. the fasted person where that fat is being turned over very quickly.”

10/ I was walking outside at the time of listening to this podcast and literally stopped in place when I heard this next part...

11/ CMJ: "... what we do have is studies where we look at labelled tracers and that's what shows that in a random sample of NASH people you have a 75 percent decrease in ApoB secretion. It doesn't matter what the ApoB in the blood is… you'd like to know why it's higher."

12/ CMJ: But you know that it's not because it's coming out of the liver-
PA: It's not secreted higher. That's a great point, right. It can be longer residence time of the VLDL, the LDL.

13/ It's hard to emphasize how meaningful this exchange is. Again, I'm fans of both @PeterAttiaMD and @ChrisMasterjohn. Regardless of prior discussions before this podcast, this exchange right here is absolutely fundamental to the energy model I propose...

14/ ... The high frequency of testing is what allows us to see the both LDL-C and LDL-P in this particular light when controlling for other variables. It's the "running video", as it were.

15/ And again, three day average of dietary fat vs LDL-P (all ApoB, of course)

16/ I know many will see this in a debate victory/loss perspective, but I don't want that. This is a conversation that just takes a long time. And whether this idea develops with me in the room or without, I just want it to move forward. It's so incredibly important to us all!