2/ Points 1 and 2 go in line with what I'd expect. Leaner metabolically healthy people probably have greater metabolic flexibility, resulting in better shift to fat burning. But point 3 about AMPK surprised me. Here's why...
3/AMPK is the cellular energy sensor. It's activated, in part by low energy status, i.e.
Decrease cellular energy supply increases AMPK activity
Seems paradoxical that in lean persons who r fasting AMPK activity goes DOWN, not UP, as if there is more energy when taking none in
4/ "Surprisingly, AMPK-Thr172 phosphorylation, which was not different between groups at baseline, was reduced by fasting in lean but not in obese"
5/ Then in the discussion the speculate that this could be due to increased glycogen stores during a fast!!! Isn't that odd?!
I find that interesting because I actually find I have a lot of power after a fast, e.g. I could more easily do muscle ups clap push-ups etc. That's n=1
6/ There is further interesting speculation as to mechanism/rationale & I encourage people to read this paper. Fun!
But one think I will point out is the they only looked at skeletal muscle AMPK. I'd bet you'd see VERY different things looking at fat cells and liver cells.
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1/ It's been quite a week on Twitter regarding #lowcarb and LDL
I have been on the fence about weighing in, not wanting to add to the dog pile, but decided 2drop my thoughts in this thread
If u don't have time to READ THE WHOLE THING IN CONEXT, ignore& consider me🪰 on the wall
2/ I'll first address @deirdre_tobias analysis of LDL and all cause mortality. With the caveats that I'm not an epidemiologist &hope to have more insightful questions when time passes and the dust settles, I am not in disagreement w/ the main results: high LDL associated with ACM
3/ That's actually old news, isn't it?Not so say that the analysis doesn't bring something to the table, but on a population level v high LDL levels (will get to low LDL in a minute) are generally undesirable. Thus, all things being =, a conservative gambler would pick low-is LDL
1/ As a #LMHR and close colleague of @DaveKeto I feel compelled to jump in here and clarify my own stance on LDLp and ASCVD risk because I feel that our positions are usually misrepresented by others. Here we go…
2/ To cut to the chase, outside the low-carb lipid triad of high LDL and High HDL and low TG, I would absolutely personally consider elevated LDLp an issue. Where I to have high LDL and atherogenic dyslipidemia I would both take an LDL lowering med and, more importantly IMO…
3/ change my lifestyle to improve the atherogenic dyslipedmia. Personally I do have concerns about longterm safety use of statins specifically and would preference Zetia/PCSK9i. But that’s besides the point. I won’t speak for @DaveKeto but for my part the LMHR phenomenon & LEM…
Thread about Twitter culture re #LCHF
1/I put up a thread yesterday about a graph depicting obesity rates over time as relates to the DGA that ended up precipitating some interesting discussions with esteemed experts.After several attempts at clarifications, I removed the tweet
2/ I removed the tweet, but it was an interesting moment upon which I wanted to reflect. I re-read it before deleting it though and, while it could have been better, when I compared to some of the replies there was a mismatch in content, at least IMO. But
3/ But is that the reader’s fault, or my own for not anticipating that my tweet would be read through a particular filter?I think it’s an unfortunate reality,but a reality nonetheless, that when one has a decent following they should realize that their tweets r going to be read
1/ BOOM! Want to know how fat gets directed to muscle, cardiac, and adipose tissue...
ANGPTL3-4-8 model of fatty acid trafficking! So elegant! It's like evolution is an engineer .@DaveKeto .@Ad_SotoMota
Video Here 👇👇
2/ The model describes how three ANGPTL family members act in concert to promote tissue-specific LPL activity corresponding to the body’s nutritional status. Interestingly, all three proteins are LPL inhibitors; however, they are differentially induced by fasting and feeding ...
3/ ...and preferentially effect different tissues. ANGPTL4 is induced by fasting and inhibits LPL specifically in adipocytes, directing direct FFA to skeletal and cardiac muscles in the unfed state. By contrast, ANGPTL8 is induced by feeding and...
Today @harvardmed we started metabolism, metabolic regulation, and had a carb metabolism lecture...
I've had a handful of peers (6 thus far today), unprompted, contact me to ask some version of the following question...
2/ I've very intentionally kept a low profile, and I'm not looking to make "my thing" (metabolic health) the focus of lectures not get myself a troublemaker label. Plus, I'm genuinely happy to use listen and learn.
BUT...
3/ I'm incredibly excited to note that my peers are asking what I personally think should be the obvious questions -->
e.g. Why treat a disease of high blood sugar and high insulin with carbs and insulin?
I find it very informative. But now, one of two things could happen...