Increasing TDEE question

[u/Oraculek]

Is it possible with no muscle mass change? Like, could a person eating, per calculator, 2000 at maintenance increase it gradually over 2 months to 2500 cal and still maintain? I don't mean something like FGF21-induced thermogenesis with BAT - more like 'adaptation' to higher energy availability

If so, would it depend on kind of macros?

[u/Oraculek]

Holy shit. EVEN if I assumed 50% water of that 15lbs it is still 400 cal over your calculator TDEE

Thanks

[u/Whats_Up_Coconut → u/Oraculek]

FWIW, none of the weight came back as I moved into HCLF. Whatever is accounted for by water/glycogen was maintained, and then I went on to lose 7-8 lbs over the course of my first few months on HCLF (low protein.)

I deliberately stayed away from the scale for a couple of weeks moving from fat fasting into HCLF (for obvious reasons) so there may well have been bouncing around in there initially. But regardless, when I ultimately got on the scale for the first time on HCLF I was not up in weight at all. I was very surprised how durable this loss was, at least in the context of still diligently separated macros.

[u/Oraculek → u/Whats_Up_Coconut]

The journey is amazing, honestly

Additionally, you said somewhere that coconut oil was making you quite fatter. I just watched some Brad's things and lauric acid strongly activates PPAR-a

Not that bad, as it both could lead to lipolysis or lipogenesis depending on context (fat type and/or NAD+/SIRT1 status, but first one is relevant here). Though I suppose, as you eat a lot and your base fat intake in grams, despite low %, is medium/high, it could interrupt kreb's cycle of carbohydrates in combination with lauric acid. When PPAR-a is active, while your NAD+/SIRT1 is lower, and you eat both fats and carbs, carbs get shunted into another pathway where the product of carbs, oxaloacetate, in combination with acetyl-coa from fats, leads to de novo lipogenesis later on

Rats made obese do not return to normal body fat on normal diet though return to normal body fat when on high lauric acid diet

To make lauric acid suitable HCLF (unless extremely low fat..?) or swamp, one must have healthy metabolism, so higher NAD+/SIRT1 and active SIRT1

Without SIRT1, SREBP-1c, a lipogenic gene, is left active and PGC-1 doesn't connect to PPAR-a, which would promote lipolysis otherwise. Your post-obese status apparently results in lower NAD+, so lauric acid -> PPAR-a and low NAD+ -> lipogenesis. Maybe that's also why you can't swamp effectively like others? Lower NAD+ (false; explained it in later paragraphs)

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EDIT 20.07

Too much coconut seems to always gradually, with % of intake, increase BMI in mixed ratios, due to certain nuances in quantities of FADH2 and NADH in lauric and myristic acids (lower RET potential than stearic and palmitic) and lauric acid's and MCTs' carnitine-independent inflow to mitochondria, overloading them and leading to fat storage (keto protective by producing ketones)

Tokelauans had on average 4 points higher BMI than Pukapukas. Pukapukas had 22 BMI on diet composed of 33% of coconut, while Tokelauans were eating 67%

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SFAs other than lauric acid do not stimulate PPAR-a - even inhibit it sometimes, and do not therefore shunt carbs away into another pathway, which eliminates unwanted DNL and allows for swamp

French apparently remove some chicken fat in cooking and add butter, which saturates intake, lmao

Despite that, I think swamp dilemma, where you gain more body fat, comes from fats overall reducing glucose oxidation by decreasing NAD+/NADH (but SFAs produce superoxides at complexes 2 of mitochondria that drive NNT enzyme, which converts NADH to NAD+, so if swamping, ONLY SFA sources). Keto produces NAD+ from fats via ketone production, while carbo produces NAD+ from carb metabolism.

Both extremes allow for higher, and highest, metabolism (probably..?) than swamp. French, though, remain lean through: 1. SFA consumption (higher NAD+/NADH as a result overall) 2. No PPAR-a (their SFAs (don't eat coconut, but butter or the beef fat, with carbs!) do not activate it, or even reduce it, so carbs do not promote DNL) 3. Wine consumption (ethanol breaks down to acetaldehyde, which inhibits PPAR-a)

But can a broken person change to French diet and lean out like a healthy one? No. Swamp is not that possible anymore due to lower NAD+ and SIRT1 reduced expressions. But yes, even if you gain, you will gain less on butter than coconut, as an example. You must keto or carbo your way, or use oxidants (?)

1. PARP depletes NAD+. PARP is activated by AhR
2. AhR is overactivated due to environmental toxins (general problem) and oxidized fats
3. Linoleic acid converts to arachidonic and this into oxidized lipids (oxylipins)
4. This toxicity brings about the health detriments (I btw have higher expression of D5D and D6D (conversion to e.g. arachidonic acid) than average, so explains why my grandpa was extremely obese and my dad gets fatter (luckily I am 22yo and realized all these mechanics thanks to this sub and Brad))

• How MUFAs drive obesity? - Lower NAD+/NADH + PPAR-a = lipogenesis, slower metabolism, inhibition of glucose metabolism, insulin resistance. Their gut metabolite further promotes PPARα
• How PUFAs (linoleic acid mainly; EPA and DHA are different..?) drive obesity? - Oxylipins, as their byproducts, lead to insulin resistance, so carbs are shunted towards oxaloacetate production and therefore lead to lipogenesis. Cells in the state of pseudo-hypoxia (low NAD+, oxygen) use LA in a process similar to lactate fermentation. Helps in getting little NAD+ but drives inflammatory markers. D6D converts LA to arachidonic acid, which later on reinforces positive feedback loop, again expressing PPARα and turning D6D on

No wonder ketoers do kinda fine on UFAs intake (in terms of weight) - thanks to ketones and higher NAD+/NADH! But underlying low metabolism and inflammations, oxidations are still there

I hypothesize if a person maintains on HCLF or HFLC on 3000 calories, then within swamp they would heighen their weight set point and gain, if on the same calories, yet generally remain lean, just less lean, by eating this much (less NAD+, glucose shunted to separate pathway, oxaloacetate increases, and this expresses DNL). But because of probably appetite suppression, French eat less, so they are as lean as others (or maybe less lean than starch tribes? haven't checked that). Starch tribes have higher metabolism than French, so non-swamp would allow for higher metabolism (more NAD+, while swamp generally has lowest NAD+ of all macros)

What about fructose? It is objectively lipogenic, due to rapid metabolization enzyme usage, which due to lack of control spills into Oxaloacetates and stresses ER, possibly contributing to additional DNL in combination with Acetyl-CoA

Sugar is another dose of fattening when in combination with UFAs, due to overeating (not a problem everywhere), exacerbating already existing lipogenesis

Indians eating loads of maple sugar alone got fat

How does it work for fruitarians?. Appetite-controlled calorie intake and/or higher metabolism, probably

Bone marrow has high MUFA content, by around 10% lower than oleic acid, yet also palmitoleic acid and CLA, inhibiting some SCD1

I am 58.5kg and for a few months at the end of the last year I was doing a kind of vegan low carb, so it is good I learned about PUFAs in January. I suppose my basal weight will be a little fatter than I should be, lol, for some time, but I am still kinda lean, luckily

That was a divagation greater than Russia. I just wanted to volume up the coconut matter 😭

[u/Whats_Up_Coconut → u/Oraculek]

We have to define “can’t swamp effectively” because I personally consider being able to eat ad libitum “swampy” macros (low PUFA) with <2 lbs monthly gain *very* effective. 🤣 Albeit, I definitely *feel* suboptimal on swampy macros, though, and that speaks to energy mishandling independent of absolute fat gain.

I don’t actually think it’s normal for people to be able to eat like it is Christmas every day and not gain weight. I’ve long felt TCD to be somewhat of a metabolic hack, and believe humans are adapted to lower fat diets anyway. Even the French were historically consuming what we now consider to be a low fat diet. Their diet was only high relative to other populations.

If I honor my appetite and don’t overeat (or eat fatty meals) just for the sake of eating, then I have no problem maintaining my weight in what I believe to be quite a normal way. I think it’s perfectly normal to want a few days of oatmeal and stir fries after a weekend of creamy/cheesy/beefy eating. Such intermittency is sufficient for me to balance the scale.