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?
4/ Yes, there is... you can announce to the room you'd like them to take less food unless they, themselves are especially hungry.
You're applying the breaks globally, yet allowing for individuals to veto this action locally.
That's effectively how ANGPTLs work
5/ Which is why there's been greater focus on this important aspect of regulation for Lipoprotein Lipase and how central it is to the #LipidEnergyModel (#LEM)
And yes, unsurprisingly, diseases that impact ANGPTLs and/or LPL have a clear impact on their resulting lipid profiles.
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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)
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.
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.
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.
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...
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
The tl:dr -> There's more selective control with fatty acid exchange in tissues than we fully understand... but we have a lot more we've learned recently...
2/ "Preferential uptake of FAs into high demand tissues such as the heart, muscle and brown adipose tissue cannot be achieved by non-specific uptake, which would acutely distribute FAs equally into all cells."
- Translation: there's some selective trafficking going on here.
3/ "A second uptake process modulated by activity of capillary lipoprotein lipase (LpL) involves FAs derived from triglyceride (TG) rich lipoproteins (chylomicrons and very low density lipoproteins." (VLDL)
- Yes, lipoproteins + LPL = hydrolysis of TG to cells