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…
4/ Are about performing research at the boundary of the unknown. The fact that LMHR are “a unique subset” given their metabolic health and absence of known genetic conditions make us a perfect natural experiment for studying the independent causal role of LDL in ASCVD…
5/ In other words, LMHR could be (maybe) the exception that redefines the rule and advances our understanding of the biggest chronic disease killer (other than last year) of Americans. Intellectually speaking it’s a fascinating phenomenon that deserves to be studies. Furthermore
6/ the advancing and evolving Lipid Energy Model #LEM serves as the basis for testable hypothesis that can should and will be the topics of upcoming studies. We have much to learn and #LMHR provide that opportunity. In the end I believe study of #LMHR will majorly advance our
7/ understanding of ASCVD and lipidology and thereby save and/or improve millions of lives
And if I were to issue one call to action it would be: “let’s unite behind science and move forward learning together (respectfully)”
8/ If you’d like any further clarifications on my stance, I have no problem being direct. @MichaelMindrum and anyone. Cheers and have a great thanksgiving
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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...
Full after fruit?
1)That’s an atypical satiation response 2) The is probably accurate bc of what the peach 🍑 would replace 3) most modern fruit isn’t “natural.” 10,000 gen of selection for sweetness … 4) Ppl would also lose weight eating more hard boiled eggs 🥚
5) of all fruit, I think peach isn’t a “bad” choice, and I’m not anti fruit. But the notion that fruits are healthy by virtue of being fruits is problematic. Most people think dried fruit is healthy, including dried 🍍 at the extreme. May as well be eating sour patch kids…
6) again, I’m not anti-fruit but let’s try to discuss in what context the fruit is being consumed and how “processed” the fruit is re artificial selection or other processing. Let’s also discuss the actual nutrient content and other options…
1/ Another in my biology series of How it Works. This time... How Does You Body Get Rid of Excess Nitrogen? #Protein
The short answer is that it transforms the nitogenous group (amino group) into urea, and it gets peed out. But let's dig in a bit...
2/ The first step is to get the Nitrogen-containing amino group off of the donor amino acid. This is done by a "transamination reaction" in which transaminase enzymes effectively shuffle the amino group, transfering it from one donor amino acid to an acceptor alpha keto acid...
3/ Again, just a simple shuffling. In the example shown Alanine is the donor amino acid, and it's amino group is transfered to alpha-ketoglutarate to make their respective alpha keto acid and amino acid pairs: Pyruvate & Glutamate...