The Mysterious Case of Pufa Depletion
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Ray recommended the slow approach.
-Remove PUFAs from the diet
-More carbs
-Antilipolytics (B3, aspirin, etc.)
-Other “saturators” (such as policosanol and perhaps the ones you mentioned)
-T3 supplementation(which has a PUFA-depleting effect when you've already limited them in your diet)That way, you limited the PUFAs’ access to the mitochondria and could safely eliminate them through glucuronidation.
The effect is the same as what I mentioned in one of my earlier comments. If a sample were taken, the tissues would have very low levels of PUFAs, so you could eliminate them in a controlled manner, which isn’t the case for most peaters, since losing fat isn’t really a concern for most of them. In that case, every time too much stored PUFAs were released, the situation would change.
If someone has the patience to wait 4–6 years for that, I don't see why they shouldn't plan for gradual weight loss as well. You can easily lose 10–20 kg over that time without even worrying about it. Peaters madness
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@alfredoolivas @texugodomel ive been digging thru some of yalls posts and twitter and it looks like im not the only one on this pufa depletion journey lol
can someone explain whats going on with this fella here^^? seems like he would be pretty saturated by now? is he on thyroid medication?
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fuck nvm he's high starch
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@hcwilliams how much weight have you lost
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@alfredoolivas 20lb including water weight
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Is there any supporting evidence for these claims? If by lipogensis you mean the creation of saturated fat from glucose then yes of course this can greatly help dilute stored PUFA, ray veven recommended this. But despite it, it still takes years to achieve dilution from what I understand . It’s also a small amount and not significant.
Lipogenesis is not creating "saturated fat from glucose." This is a massive misconception. Lipogenesis creates Palmitic Acid (which is a saturated fat) from Acetyl-CoA and Maylonyl-CoA (which itself is created from Acetyl-CoA). Those Acetyl groups can come from any energy source- glucose, fructose, Krebs cycle intermediates, alcohol, and (the big one) other fats. Studies frequently show that a high fat diet activates Fatty Acid Synthase more than lower fat diets. Many fats, especially PUFA and Omega 3 fats, undergo "carbon recycling," which is breaking down the fat into Acetyl groups, and then rebuilding them into safer fats like Palmitic Acid. FAS only creates palmitic acid, but there are other enzymes that can elongate and desaturate it.
A lower fat, high carb/sugar diet will use most of those carbs for energy, while circulating PUFA will be broken down into acetyl groups, and then rebuilt into palmitic acid. So, the process is much more direct, and not all PUFA will be burned as PUFA, some will be broken down and rebuilt into SFA, and some will be excreted.
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@ZackVegas thanks for that
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@hcwilliams amazing work
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@alfredoolivas thank the DNP
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@hcwilliams legend
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His approach is based on almost the same idea as most others: that if you restrict PUFAs, you’ll deplete your body’s stores within 4 to 6 years, so the main idea is that excess omega-6 is the “cause” of obesity and that depleting it would properly adjust the system and lead to a normal, healthy weight without having to force calorie restriction; almost all of his experiments with diet are carried out without controlling calories
Without actively aiming to deplete total body fat, you’re at the mercy of how correct the theory is; at best, weight loss will accelerate the closer you get to the 6 year mark; at worst, you gain weight because, although PUFA might have been the initial trigger, the other “broken” parts also become independent triggers
I like the experiment because it provides data, but I stand by my view that without losing body fat, you may never reach the desired state just by merely restricting PUFAs
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@TexugoDoMel kinda figured that was the case. I think Buddy still needs thyroid or some sort of intervention at this point too or he’ll never be a 120 year old Lean Balkan dairy farmer
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