1/ Posting this hypothesis for posterity:

I now suspect #PlantBasedLowCarb (PBLC) isn't as low carb as originally thought.

Before getting started in this thread, I should emphasize I wouldn't consider this a good or bad thing in and of itself, but it is of interest, ofc... Image
2/ Moreover, I've regularly pointed to people following my work who are both (1) very interested in a low carb diet, but (2) would prefer to keep their #LDL low to consider PBLC as a "third option", as I commonly see it associates with this outcome.

Now to my hypothesis...
3/ PBLC generally has two major features separating it from "typical" #keto/#lchf:

1) More fat sourced from mono and polyunsaturated fatty acids (M/PUFA) instead of saturated fatty acids (SFA)

2) A lot more soluble and insoluble fiber via plants
4/ It's generally assumed one can easily achieve being keto on plant-based given blood levels of beta hydroxybutyrate (BHB), a ketone body, tend to be high on PBLC.

But here's the thing, PUFA is very "ketogenesis-inducing" -- (@KetoCarnivore has a lot of material in this area)
5/ There are a number of studies that explore this, such as this one (though not that ideally): academic.oup.com/jcem/article/8…

But this begs an interesting question...can PUFA being more ketogenic actually mislead us into assuming lower glucose, higher fat use than expected for a diet?
6/ In other words, can a diet *appear* to be more ketogenic due to the higher use of PUFA in spite of marginally higher carbs?

I think so.

Remember, BHB (like glucose) is a substrate in the blood...
7/ Like many substrate blood tests, we are measuring that which is in transit, but not yet in use. We can't know for certain what the actual secretion and/or uptake is.

So we don't truly know how much BHB will correlate strongly with actual fat vs glucose use by cells.
8/ Which brings me around to my hypothesis regarding fiber, particularly soluble fiber.

I posit it may appear less glycemic than it is due to a greater use of M/PUFA generating BHB under this PBLC context.

There are two metrics that would help test this...
9/ The first is Respiratory Exchange Ratio (RER). Never mind resident ketone levels in the blood, looking to the aggregate cell respiration itself will certainly give you a powerful metric of what degree a usage each substrate is providing.
10/ The other is a Continuous Glucose Monitor (CGM), which I likewise believe will show marginal, yet detectable changes in my glucose levels.

I plan to do each of these for my coming fiber-only intervention experiment. Should be fun to see how these results play out.

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More from @DaveKeto

25 Sep
1/ New #LipidEnergyModel video on ANGPTL proteins via @nicknorwitz

And a few added thoughts...

ANGPTLs are *all* inhibitors. They are applying the breaks to the Lipoprotein Lipase (LPL) in particular.

So consider this analogy...
2/ Imagine a room full of people at tables being served with trays of food regularly coming from the kitchen moved around the room by waiters.

No one is particularly famished, but they aren't especially full either, so they are absently taking food off the trays to maintain...
3/ However, a few guests at one table leave to get some exercise and return quit hungry.

And here's the catch: You can't tell specific people to do specific things (including the waiters), but you can say things to the entire room. Is there a way to solve this puzzle?
Read 5 tweets
16 Sep
1/ Okay, finally getting around to this experiment video by @ScepticalDoctor

Naturally, this has many things I'm interested in -->
- N=1
- #Lipids (esp #Cholesterol)
- and not least of all, Anna and I have many respectful, kind debates (more of that plz, #NutritionTwitter)
2/ "But this experiment is mainly for entertainment purposes. Self experiments like this are irrelevant from a scientific perspective."

Unsurprisingly, I do disagree on this wording. I think it's fair to say self-experiments have "limited" relevance (depending on design)...
3/ ... But a well designed N=1 can provide quite a lot of scientific value, even if primarily hypothesis-generating.
Read 15 tweets
5 Sep
1/ Yes, my answer to the poll by @nicknorwitz was "Gain 4% body fat". And honestly, it was a pretty easy one when compared to the others.

But to be fair, I also have quite a bit of direct data on this in particular... let's unpack...
2/ First, if you didn't already know this about me, in 2018 I literally gained almost 20lbs of fat for the Weight Gain Experiment. cholesterolcode.com/weight-gain-ex…

(As an aside, I realize now I did presentations on the findings for this experiment, but didn't do a write up. Bad Dave!)
3/ But spoiler alert -- my total and LDL cholesterol did indeed go down where having gained weight and back up where having lost it.

To be sure, I think there are thresholds to "active fat gain/loss" vs standing, stable fat mass, but we'll save that for another thread.
Read 8 tweets
2 Sep
1/ Wow -- it's been quite a week! I announced the #LMHRstudy six days ago. And in case you missed it -- visit here for more details:

CitizenScienceFoundation.org/study

I'm going to provide some updates and answers to frequent questions of the last several days...
2/ "Dave, can you get me in the study?"

No! You have to contact Lundquist directly through the proper channels and they will decide based on the study design whether you qualify as prescribed by existing eligibility criteria we all determined in advance.
3/ While myself, @DrNadolsky and @DrRagnar developed the protocol in collaboration Lundquist, we in no way can (or should) influence any decision making regarding individual considerations -- and that's a good thing. We want this study as fair and objective as possible.
Read 7 tweets
6 Aug
1/ Okay, let's talk ANGPTL3-4-8 model. Mega thx to @nicknorwitz for getting well ahead of me on the angptls and their influence on LPL.

Here's the central figure, which we'll be referencing.

(Don't worry if you get lost, I'll unpack this more below..)

royalsocietypublishing.org/doi/10.1098/rs…
2/ "Lipoprotein lipase (LPL) is a rate-limiting enzyme for hydrolysing circulating triglycerides (TG) into free fatty acids that are taken up by peripheral tissues."

Translation: LPL is like a key cells use to open lipoprotein boats to offload their fat-fuel cargo (TG)
3/ "Postprandial LPL activity rises in white adipose tissue (WAT), but declines in the heart and skeletal muscle, thereby directing circulating TG to WAT for storage; the reverse is true during fasting"

Sure, post-meal we do more storing in fat via LPL, otherwise we do less.
Read 11 tweets
5 Aug
1/6 I'd like to both retweet and add on to @NutritionMadeS3's point here...

Again, and with emphasis, my position is one of cautious optimism. That's an explicit acknowledgement of uncertainty, even if I have a leaning toward the positive in this context...
2/6 I discuss this at length in 13-15 of my pinned tweet

Hence the importance of #LMHRstudy

I'd hope this were self-evident, but if I were completely certain high LDL + high HDL + low TG = low risk in fat-adapted context, there'd be no effort for a study
3/6 I've chatted with @NutritionMadeS3 and others on evidence I consider very compelling regarding the connection of health and illness for lipid metabolism and their impact on lipid profiles. But I likewise stress we'd be better served with prospective data in this context
Read 6 tweets

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