The Mysterious Case of Pufa Depletion
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Very low-protein days followed by high-protein refeeds—using an alternating schedule (one day restricted, the next not) or a "protein refeed" after every two days of restriction.
As you probably know, there is a study that shows the triene/tetraene ratio rose was inversely correlated to protein intake
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Stearic acid supplementation, since a significant portion converts to oleic acid, which accelerates tissue PUFA depletion through competition.
Could you expand on this?
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Very low-protein days followed by high-protein refeeds—using an alternating schedule (one day restricted, the next not) or a "protein refeed" after every two days of restriction.
As you probably know, there is a study that shows the triene/tetraene ratio rose was inversely correlated to protein intake
Yeah, restricting protein generally reduces desaturase activity. The result is a drastic decrease in unsaturation due to the limitation of PUFAs with multiple double bonds (caused by the downregulation of delta-6 and delta-5 desaturases); consequently, if the restriction continues, delta-9 desaturase activity eventually increases to prevent unsaturation levels from dropping excessively.
With delta-9 desaturase making more oleic acid available, a greater amount of oleic acid proceeds to the delta-6 desaturase, "winning" the competition against linoleic based on sheer quantity.
My theory regarding protein restriction and refeeding is that the refeed phase following restriction causes a massive spike in desaturase activity; if PUFA intake is limited, this creates an excessive flux of oleic acid being converted into Mead acid
Stearic acid supplementation, since a significant portion converts to oleic acid, which accelerates tissue PUFA depletion through competition.
Could you expand on this?
Unsaturated fatty acids (UFAs) compete with one another for enzymes and space (such as within cell membranes); therefore, increasing the level of one UFA inevitably reduces that of another once a certain threshold is crossed.
There are basically two ways to accelerate n-3/n-6 depletion, and both involve drastically increasing oleic acid levels:
- Accelerating delta-9 desaturase activity to boost the conversion of stearic acid to oleic acid; this is typically achieved through cycles of fasting and fat-free refeeding.
- Increasing oleic acid intake while on a PUFA-restricted diet.
Regardless of the diet, the body converts almost all stearic acid into oleic acid. Since it is generally difficult to find an oleic-rich food that doesn't also contain excessive amounts of linoleic acid, the best approach I’ve found is direct stearic acid supplementation; this allows you to increase oleic acid levels in proportion to the amount of stearic supplemented while adding zero PUFAs.
- Accelerating delta-9 desaturase activity to boost the conversion of stearic acid to oleic acid; this is typically achieved through cycles of fasting and fat-free refeeding.
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@TexugoDoMel
Macadamia oil is the only oil I can think of that's high in oleic acid and low in PUFA. Downside of course is the high price.I've never been a big party attender, but I never went to a party where I didn't probably offend most of the people there by talking about what I was interested in. (Ray Peat)
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@Luke Helianthus Annuus Hybrid Oil. Cheap and available. 3% PUFA, 88% MUFA, 9% SFA.
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Helianthus Annuus Hybrid Oil
Is that the same as High Oleic sunflower oil?
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@TexugoDoMel these are good theories. Especially the stearate and oleic acid one. PUFA depletion black pill kinda
I’ll personally lean towards more PUFA being burned from a higher metabolic rate. Would I be wrong?
Unrelated, but could you try to explain to me the glycine to methionine ratio? Like why does it matter in terms of protecting against the harmful metabolic effects of methionine.
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well, the inspiration came from this quote on a GE podcast. Georgi: What about chemical interventions? I mean, there is a tremendous track record of things like dinitrophenol being able to cure effectively even extremely morbidly obese people, of course, under medical observation because it can easily kill you if you overheat. Wouldn't something like that be considerable?
Ray: Overdosing on thyroid does the same thing. At the right level, it can increase your safe oxidation of fats while helping to suppress the toxic or random oxidation. Both DNP and thyroid can carefully controlled can reduce the toxicity of getting rid of the fat.
But again thyroid overdose per se would render my cholesterol to undetectable levels. DNP even in high doses doesn’t seem to have that effect on me.
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This post is deleted! -
@hcwilliams why did you delete your comment bro lol
If you aren't afraid of DNP, you shouldn't be afraid of a low/moderate dose of androgens. They are SUPER effective at preserving lean mass. Especially, if you aren't on thyroid :). I believe they also increase the triene/tetraene ratio
Ill try to find the study -
alfredoolivas said:
triene/tetraene
Using 20:3/20:4 ratio, (it wasn't clear what 20:3 fatty acid was studied, was it mead or DGLA?)
1.33 Control slow moving lecitihin
0.88 E slow moving lecitihin
1.57 T slow moving lecitihin1.57 Control fast moving lecitihin
0.97 E fast moving lecitihin
1.3 T fast moving lecithinhttps://pubmed.ncbi.nlm.nih.gov/5910280/
Idk if this is substantial. Probably not.
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@TexugoDoMel
Macadamia oil is the only oil I can think of that's high in oleic acid and low in PUFA. Downside of course is the high price.Macadamia oil is good, and I use it sometimes, but since the total percentage of PUFAs in the diet is at the top of the hierarchy, it still contains a lot of linoleic acid. Supplementing with stearic acid doesn't add to that and helps lower the (n-3+n-6)/(SFA+MUFA) ratio even further.
@TexugoDoMel these are good theories. Especially the stearate and oleic acid one. PUFA depletion black pill kinda
I’ll personally lean towards more PUFA being burned from a higher metabolic rate. Would I be wrong?
Unrelated, but could you try to explain to me the glycine to methionine ratio? Like why does it matter in terms of protecting against the harmful metabolic effects of methionine.
It’s not exactly a theory, since it’s been demonstrated in animals, haha. You can combine various approaches, but the main thing should be to keep your metabolic rate high, IMO as well.
I’ve never really paid much attention to it, but since glycine is involved in the methionine cycle, I’d expect it to help regulate methyl levels (GNMT?), helping to dissipate excess methyl
From "Protective CO2 and aging"
well, the inspiration came from this quote on a GE podcast. Georgi: What about chemical interventions? I mean, there is a tremendous track record of things like dinitrophenol being able to cure effectively even extremely morbidly obese people, of course, under medical observation because it can easily kill you if you overheat. Wouldn't something like that be considerable?
Ray: Overdosing on thyroid does the same thing. At the right level, it can increase your safe oxidation of fats while helping to suppress the toxic or random oxidation. Both DNP and thyroid can carefully controlled can reduce the toxicity of getting rid of the fat.
But again thyroid overdose per se would render my cholesterol to undetectable levels. DNP even in high doses doesn’t seem to have that effect on me.
The comparison they make between DNP and thyroid is because DNP increases the metabolic rate exclusively through uncoupling, while thyroid increases both ATP production and uncoupling. He just gave the example of a thyroid overdose to illustrate the ratio of uncoupling to the increase in ATP production.
I still think thyroid is better, and as I said, you don’t need anything close to an overdose
alfredoolivas said:
triene/tetraene
Using 20:3/20:4 ratio, (it wasn't clear what 20:3 fatty acid was studied, was it mead or DGLA?)
1.33 Control slow moving lecitihin
0.88 E slow moving lecitihin
1.57 T slow moving lecitihin1.57 Control fast moving lecitihin
0.97 E fast moving lecitihin
1.3 T fast moving lecithinhttps://pubmed.ncbi.nlm.nih.gov/5910280/
Idk if this is substantial. Probably not.
I remember reading that exercise increases unsaturation in muscle tissue, but they used that finding in a questionable way because the increase in unsaturation they mention is a decrease in stearic acid and an increase in oleic acid; perhaps steroids have a similar effect
@hcwilliams why did you delete your comment bro lol
If you aren't afraid of DNP, you shouldn't be afraid of a low/moderate dose of androgens. They are SUPER effective at preserving lean mass. Especially, if you aren't on thyroid :). I believe they also increase the triene/tetraene ratio
Ill try to find the studyI’m finishing up my research (and testing) on muscle growth, but ever since I started looking at it from a more Lingian perspective, androgens have taken on a more secondary role for these purposes, serving as a sort of workaround to compensate for what actually causes hypertrophy.
Androgens seem to me to be more of a structural stabilizer; depending on the animal model of hypertrophy you look at, the (%) hypertrophy is the same in the control animal and in the animal using androgens. The benefit of androgens is solely the reduction of muscle damage, but they do not accelerate hypertrophy; both end up the same.
In fact, with this model, you can castrate and bring testosterone to nearly 0, you can suppress IGF-1 or insulin to nearly 0, and the (%)hypertrophy remains the same
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@hcwilliams why did you delete your comment bro lol
If you aren't afraid of DNP, you shouldn't be afraid of a low/moderate dose of androgens. They are SUPER effective at preserving lean mass. Especially, if you aren't on thyroid :). I believe they also increase the triene/tetraene ratio
Ill try to find the studyLol my answer didn’t make sense to your question I was responding to.
I’m on testosterone now
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@alfredoolivas is it true that after a certain dose of testosterone you stop aromatizing into estrogen because the testosterone starts competing for the estrogen or aromatase enzyme/receptors?(I butchered that)
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I remember reading that exercise increases unsaturation in muscle tissue,
This would be due to adrenaline right? I know caffeine and thyroid increase SCD 1 levels.
perhaps steroids have a similar effect
Trenbolone can supress SCD 1 levels in animals I have read, and if I remember correctly, so does testosterone.
Androgens seem to me to be more of a structural stabilizer; depending on the animal model of hypertrophy you look at, the (%) hypertrophy is the same in the control animal and in the animal using androgens. The benefit of androgens is solely the reduction of muscle damage, but they do not accelerate hypertrophy; both end up the same.
Oh yeah, I agree. think in endogenous produced amounts, their effects on hypertrophy aren't as they claimed to be. Thanks for the study
is it true that after a certain dose of testosterone you stop aromatizing into estrogen because the testosterone starts competing for the estrogen or aromatase enzyme/receptors?(I butchered that)
That has not been demonstrated, but it's plausible in theory. Testosterone itself is not the best substrate for aromatase, it's the metabolite, androstenedione, that is a better one. However, the affinity is still moderate - high.
Androgens themselves have neglible affinities for the estrogen receptors. However, especially, exogenously, they circulate at concentrations 100s of fold greater than estrogens. This neglible affinity may become relevant at these concentrations. But again, there are estrogenic metabolites such as the androstenediol and 3a & b androstanediol that have direct and weak affinity for the ERs, and activate them. So I don't think that T directly would have any anti estrogenic effects.
However, genomically, activation of the androgen receptor supresses aromatase and reduces estrogen receptor concentrations. This is why 5 AR androgens were trialed in treating breast cancer. Simply because of their epi genetical anti estrogenic effects. Not because of their direct affinities for aromatase or receptors.
And this is why the 5 AR steroids are ran alongside T - to have an androgen that has no direct estrogenic potential, that has epi genetical anti estrogenic properties, stopping the aromatising and estrogenic effects of T and it's metabolites.
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@alfredoolivas awesome thanks for the reply.
Is tren the only feasible way to build muscle during a caloric deficit? Or are there other methods?
………….(( I probably can’t use thyroid with dnp because last time I did that even <3mcg doses would punish my cholesterol and I’d get manic depressed until it came back… I also felt amazing on dnp cus of high temps))I haven’t lifted in two years so I’m skinny fat but with muscle memory and “newbie” gains I think I can have somewhat decent gains. I just really don’t wanna get low body fat and be gaunt with no muscle
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@hcwilliams you won’t lose muscle if you lift, eat enough protein and if you do steroids, any steroid, you’ll gain muscle. Especially if you haven’t lifted in 2 years. The question is whether you want a watery or less watery steroid. If you are on testosterone, I’d stick with that and assess your strength. If you are losing significant strength, bump up your dose. I can’t reccomend tren (even though I probably did) the insomnia and oxytocin increase can make it unbearable to many. I’ve litterally been surviving (and thriving) on 5-6 hours sleep on average for the past couple months.
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@alfredoolivas I have too much on the line to risk it with tren. 5-6 months on tren I bet you're a freak of nature
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not a big fan of AI but I asked it about my plan to deplete overall pufa stores then refeed with saturated fat to increase sa:pufa ratio
"You Can't Burn Your Way Out of Structural PUFA
Adipose tissue is not just a giant, homogenous bucket of liquid oil where everything mixes together equally.The "Core" vs. The "Shell": Essential PUFAs (like linoleic acid) are structurally embedded into cell membranes across your entire body—your brain, red blood cells, nerves, liver, and mitochondrial cristae. They are not sitting in your subcutaneous fat depot waiting to be mobilized; they are functional components of tissue architecture.
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The reason the 2–6 year timeline is stubborn is that true PUFA depletion is a turnover problem, not just a math problem. The cells containing the old, damaged seed oils have to naturally die off, cycle out, and rebuild their phospholipid bilayers using saturated fats and what the body manufactures itself."
this makes sense but not sure what to do about this to speed up the process of cellular pufa
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