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Dave Feldman Profile picture
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6 Feb, 5 tweets, 3 min read
Ah — looks like I have a podcast for my walk today...

... I may be adding comments to this thread as I listen...

@FoodLiesOrg @TuckerGoodrich @drcateshanahan
Had to run minute 23 Tucker brings up that there are some amount of these PUFAs that are necessary and obligate to the body, but the quantity is typically much higher in the modern diet due to heavy use of seed oils...
... I bring this up because I do think @TuckerGoodrich is often portrayed by others as though he’s against any amount of PUFA in the diet. As always, I’m #ProNuance. ;)
Add around minute 24 @drcateshanahan says that biopsies of cells around the turn of the century showed apx 2-3% PUFA content, but there are some with content around 30-35%. Didn’t know that one... I’ll reach out for linkage...
Yes! At around 47 minutes 30 seconds Tucker starts discussing how insulin is an intermediary in uptake of oxidized Lipoproteins (A subject of particular interest to me, as you all know)...

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More from @DaveKeto

Dave Feldman Profile picture
7 Feb
1/ There really has been a sea change I've noticed lately with regard to both the #LipidTriad and the #LMHR phenotype.

I'm not going to call anyone out, but I will say there are many who I had several spirited discussions in the past few years... Image
2/ ...who considered high LDL = "high" risk, full stop...

... but are now expressing #LMHRs may actually be at "low" risk of cardiovascular disease (in spite of having LDL in the 95% of the pop), just that they "could be better" if they have these LDL levels lower than they are.
3/ It's worth emphasizing their position hasn't changed with regard to higher LDL = *more risk* of CVD. Thus, it would still be better for #LMHRs to have lower LDL, all else being equal.

But the magnitude of difference in the assumed risk has changed for many.
Read 6 tweets
Dave Feldman Profile picture
2 Feb
Really enjoying this latest podcast on @PeterAttiaMD’s #Drive so far.

Now up to the part where Dr Yassine is discussing GLUT1 regulation with the brain... (about 22m in)...
Hmmm...

“... the brain is not efficient at using fat as a source of ATP.”
“... nevertheless when the brain goes through crises and cannot utilize glucose, we have a mechanism to extract ATP from fat. But the result is a price tag, the result is oxidative stress.”

Please visit this around minute 24 to get the full context.
Read 5 tweets
Dave Feldman Profile picture
23 Jan
1/ So I did my 3D body scan this morning (and no, not posting pictures or sharing absolute numbers).

This will have been 5 days since isocaloric carb swapping in low-ish carb for keto.

Waist +0.9"
Stomach +1.2"
Hip +0.4"

Wow... in 5 days? This was pretty unexpected...
2/ Just a reminder-- this is the most controlled experiment between phases I've had to date. Replicated sleep and exercise timing and patterns, even water quantity and consumption window.

Given this shorter time span for the phase, I wasn't expecting much difference to emerge...
3/ Although, to be sure, both my wife and I noticed I was putting on more weight in the midsection even before the scan. I'm holding at around 199.6 for two days in a row, so while I gained around 2.5lbs initially, it seems to have leveled off.
Read 8 tweets
Dave Feldman Profile picture
21 Jan
1/ Well... this is awkward...

I'm gaining weight on my "bonus" carb-swap phase in spite of it being isocaloric and everything else being nearly identical (exercise, sleep, supplements, even liquid consumption) w/ prior keto phases.

And I'm gaining it pretty fast, actually...
2/ And actually, the "low carb" phase is technically slightly lower in calories than the keto phase.

And this experiment is as controlled as I get
- Fixed eating times with fixed meals (9am/2pm/7pm)
- Fixed exercise (walking) with same route and time (~3pm)
- Comparable sleep
3/ Sure -- like many reading this, I'd assume this is in large part glycogen and water gain. But I'll concede this is impressively fast given I'm at maintenance level of calories -- which was literally just demonstrated in the run-up phases before this one.
Read 4 tweets
Dave Feldman Profile picture
20 Jan
1/ #ReadingThread

This paper by @zinocker, @kariannesve, @simondankel is proving an interesting read. Before I get too much further, I'm going to turn it into a "reading thread" and post some of these quotes as I go...

(Big hat tip to @bigfatsurprise) academic.oup.com/ajcn/advance-a…
2/ "In this paper we propose a novel model, the homeoviscous adaptation to dietary lipids (HADL) model, which explains changes in lipoprotein cholesterol as adaptive homeostatic adjustments that serve to maintain cell membrane fluidity and hence optimal cell function."
3/ Later in the abstract: "Hence, circulating levels of LDL cholesterol may change for nonpathological reasons. Accordingly, an SFA-induced raise in LDL cholesterol in healthy individuals could represent a normal rather than a pathologic response."
Read 15 tweets
Dave Feldman Profile picture
20 Jan
1/ Some preliminary data from the #EatingWindowExperiment while we wait for the labs to come back.

These are the mean avgs for each period taken over the last 3 days of each phase (wake/7am/9am/2pm/7pm/10pm) compared.

Needless to say, this is some fascinating stuff...
2/ I was taking glucose and ketones (BHB) via @KetoMojo, lipids via CardioChek from @ptsdiagnostics

Where my test and meal times were the same, I'd take the blood test just before the meal.

(For study design, see cholesterolcode.com/eating-window-…)
3/ Again, I'm eating exactly the same thing in each phase, exercising the same, sleeping the same, etc -- the only difference is in the 10.5hr window my meals are 5 hours apart. In the 4.5hr window my meals are 2 hours apart.

(I added the 0.5 to reflect eating time of last meal)
Read 9 tweets

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