"Skeptical of the idea that it represents a real lack, cause wtf is in chilies/tomato sauce?"
There are more nutrients than just vitamins and minerals and amino acids! Many other organic acids feed into the Krebs cycle. For example, citric acid, malic acid, acetic acid, etc are all found in foods and are used to produce energy. Tomatoes and peppers both contain citric acid, malic acid, and, well ascorbic acid is vitamin C. But for example, you need vitamin C to make carnitine to be able to shuttle fatty acids to be burned, so craving vitamin C makes sense after a fast because you weren't getting carnitine from meat but your body still had to burn fat, so it was drawing on your vitamin C. And you need plenty of citric acid to make acetyl-CoA, not just for energy production but lots of other functions (reminder that another name for the Krebs cycle is the citric acid cycle). You need malic acid to keep the cycle going, but it comes a few steps before recycling citrate so you may have just used it up that way, though malic acid does other things in the body too.
It is possible to have genetic variants that make it difficult to synthesize or recycle any of those as well, such that you may struggle if you're not eating those foods instead.
I was incredibly low in citrate when I took one a few weeks ago. I think an organic acids test could probably tell you a lot more helpful information about dysregulated metabolic pathways in your body, and maybe a full genome could help you figure out why you seem to need such a specific diet. Sometimes there are things you can do to circumvent genetic inborn errors of metabolism, like simply supplement the thing your body struggles to produce when possible, or supplement larger doses of the cofactors for your goofy-shaped enzyme that doesn't react as easily as it should, so that the chances of it reacting is much higher. For example, I have an ACAD9 problem so that I can't metabolize very long chain fatty acids and have some issues metabolizing long chain fatty acids. That is reflected in my OmegaQuant as well. Because it's involved in assembling complex I of the respiration chain and it is not an issue of producing some other nutrient, but rather difficulty breaking down what is there, my only recourse is to make the enzyme work better. Taking riboflavin makes things pretty functional, and it is *not* an amount of riboflavin I could feasibly get from food (which is typically the case with genetic stuff). I also do better with some carnitine supplementation and glutamine to work around issues with that same gene.
Very high numbers for very long chain fatty acids. They're usually supposed to be a fraction of a percent, but I'll have like three and four times the reference range that are known to cause pathologies, and I get the symptoms of it, too -- like blurry vision is the really obvious one -- if I don't take riboflavin.
The chili/tomato thing is weird, but interesting. I can imagine that you've come to associate tomatoes with protein by eating tomatoes and beef together all the time, (I think when we're in some sort of deficit we tend to crave *the taste that last fixed a similar deficit*) but I'm surprised that your appetite hasn't figured out that tomatoes/chilis alone don't do the trick yet, and focussed itself on getting more beef. Still, if it's usually true that tomatoes/chili come with protein I can see why it might stay confused.
Just in terms of numbers, I've eaten beef w/ tomato sauce about 400-500x the last 2 years, and chilies/tomato sauce w/o any protein maybe... 9 times? So my body could be forgiven in misinterpreting that signal a bit.
I noticed an effect similar to how you describe it a few years after going keto. Before keto, my typical "cravings" foods were pizza and stuff like that. About 1.5-2 years into keto, I started fasting and realized I no longer even craved these carb heavy foods when starving. I was craving steak. Definitely seems like that association is somewhat fluid.
Sounds about right, if your body has got used to 'tomato chili sauce is the taste that fixes protein deficiency' it could take a long time of 'tomatoes without protein' for that connection to get extinguished.
Operant conditioning is pretty well understood and I'm told that those associations can be very difficult to get rid of once they're made.
Still, it's no real problem, and actually a nice association to have. Tomato/chili cravings are your signal for 'I have taken my protein intake (or a specific EAA) too low'. That's a great signal to have, you really don't want to be in actual protein deficit, causes all sorts of trouble.
At that point eat some cheese. And if that makes you stop craving tomatoes (whereas actual tomatoes don't!) then you have an idea what's going on.
My normal tomato sauce has no chilies in it. There is no spicy food in ex150, not even added salt. But chilies and tomato are both weird crack-adjacent New World nightshades I think, so maybe somehow related in my head?
Yea I'd say they're definitely similar in an acidy/sour way. Another commenter also mentioned how citric acid is an input into the Krebs cycle, necessary to use carnitine or something like that. So could be that not eating beef (=carnitine) increase my requirement for citric acid, and the craving is real.
This post is almost depressing! You did multiple 5 (!) day fasts and still didn't lose weight. Are you getting concerned that you'll ever hit your target weight?
I'm actually so happy at 220ish and feel so great, I'm totally fine with never losing another pound (sustainable, we've seen I can briefly starve myself down lol).
So I wouldn't use the word "concerned." But I sure would like to understand what's causing this "settling point" or "setpoint" or whatever it is.
Me too! If a few more other intervention theories don't work, I'm starting to wonder if adding more muscle would help via strength training at this point. Are you in the skinny fat pit? What is your homa-ir (insulin & glucose)? I don't quite remember what your current dexa scan results are too and what BF% you are.
I've seen a few people get to this point where the weight loss stops, but all they do is dieting and maybe cardio at most. I know your doing the X3 bar but maybe focusing on lean mass muscle gain could be the next phase you do to get something moving, and give a long term signal to your body that it's not winter any more, time to wake up for spring.
South asian buff people are probably the best source for getting out of the skinny fat zone since they (epi)genetically have to deal with a lot of crap that makes all weight loss harder and a propensity to be skinny fat.
Also really curious what a genefood test would say at this point what your recommended diet should be. I'm guessing it's probably a very fat heavy one, but I'm also wondering what other details they would bring up.
I'm not skinny fat, I'm muscular-fat (always have been).
My insulin is slightly high, glucose typically very low although in lab draws it tends to be higher (cause I have to walk round a while before the draw?). Typically, at home, I often spend significant parts of the day/week below 70mg/dL right now. Seeing 90 is rare.
Well he *did* lose weight, almost certainly some fat even, he just put it back on again. That's to be expected if there's a mechanism trying to keep your fat percentage constant by controlling your appetite.
If that mechanism is broken by PUFAs then the only hope long term is to get the PUFAs out of adipose. You'd think that would take years, but there are people on r/saturatedfat who seem to have done it in a couple of years, I think we should have a careful look at what they did.
I would say fasting isn’t for weight loss; it’s for autophagy, immunity, etc. I’ve fasted (18:6 or 20:4) every day for almost 6 years and I basically never get sick. But it doesn’t cause me to lose weight. My spouse has similar results. Though I'm sure ExFatLoss himself will have had an opposite experience, haha.
Haha I barely consider 16:8 a fast. Just sleep is 8h. If you don't count the cream, I do OMAD. And a lot of the "fasting factors" are not triggered by pure fat (some are), like glucose, insulin (barely), and so on.
Really exciting! I'm not surprised that you put the fat back on after fasting, of course, but it's plausible that it caused you to shed more linoleic acid than usual. However I'd also expect that if that had happened it would have brought your set point down slightly and you'd have reckoned the fasting worked. I'm most interested to see how that works out next time you do a test.
Do remember that adipose LA and OmegaQuant LA aren't the same thing. The target might well be 10% OmegaQuant, but it's probably 2% adipose?
If fasting *is* a way of getting LA levels down faster I might have a go myself.
I do wonder whether losing weight and then regaining it brings down adipose LA percentages faster than just staying at a constant weight does. It would be great if it did. You make a good point that when fasting you don't have any LA coming in at all, so you'll have to draw some from adipose for essential needs.
But if I remember rightly it took George Burr's friend six months of an entirely fat-free diet to get his LA from 4% to 2%, and I think that was serum LA (no red blood cells). If that's true then a 2% drop from ten days of fasting seems far too good to be true. (https://theheartattackdiet.substack.com/p/the-george-burr-diet)
In reading your comment, I wonder if it was actually the fast that brought down the OQ LA by 2% or if it was the fact that I basically haven't lost weight in half a year. With 3-4 months of lag in RBCs, maybe it just became "visible" right now, either because of the fast or maybe even a coincidence.
If that's true, my next OQ (already in the mail) should still be pretty low, and I suppose I should then start losing weight again soon? Speaking of predictions.
Yeah, could be, I imagine that losing weight you lose both ordinary fat and PUFA pretty much in proportion, and so the LA percentage stays constant, but if your weight is stable and you're not eating any PUFAs the percentage should come down.
So I can well believe that you've lost a couple of percentage points of LA over the last six months, just like George Burr's friend did on his totally fat free diet.
Unfortunately for ideas about 'PUFA blood levels interfere with homeostat', though, I'd figure that your 'set-point/settling-point/fixed-point/equilibrium' level should have shifted slightly downwards as a result, so you should have already got the benefits. Maybe not much, but it should be there. I can't see why it would lag.
But it's got to be more complicated than that, because everyone who's ever lost weight for any reason seems to report plateaus mixed in with sudden drops, so maybe there's some hysteresis somewhere? Perhaps the actual rate of PUFA release is variable for some reason? Or maybe some receptors somewhere are permanently damaged and need to die off and be replaced to start working again?
At any rate, if 'PUFAs involved in obesity in any way that can be reversed', I'd definitely expect your weight to be going down slowly over time, at least looked at medium-term, as long as you don't change what you're doing. And it doesn't seem to be doing that at the moment, I agree.
I'd be interested to see what happens if you go back to ex150 for a month. I'd predict a weight rise, and then if you go back to ex115 it should come off again. In both cases it should look like an exponential decay I'd imagine, but it would be interesting to see if there were plateaus or if it just happened smoothly.
I'm doing ex150 right now, so your wish will come true and we will find out haha.
Agreed on the "complicated," it really depends on what the mechanism even is. Is it that cells built w/ excess PUFAs don't burn energy good and send bad signals? Then it might depend on which type of cells we're talking about. Brain cells reacting to leptin? Other brain cells? Cells producing leptin? Mitrochondria? Mitochondria of which cells?
> I'm doing ex150 right now, so your wish will come true and we will find out haha.
OK, since I believe that protein is somehow directly involved in this hypothesised set-point-shifting, I will boldly predict that your slight increase in protein intake will lead to a slightly raised set-point, which will result in just enough extra hunger to cause your weight to go up a few pounds, probably in an exponential-decay sort of pattern.
And then if you go back to ex115 afterwards, that will reverse and you'll go back to where you are now. (Or maybe a bit lower because of two more months of PUFA-clearing)
RBC phospholipids themselves are probably not that interesting. RBCs are pretty inert. In mammals they don't even have a nucleus so I don't think there's much going on there at all. They might just be little bags.
Excess PUFAs in the membranes might shorten the lifetime of the cells by oxidising or something, but they might also make them a bit more flexible so they squeeze through capillaries easier and mean the heart doesn't have to work so hard to pump them through a damaged circulatory system.
I'm more interested in the PUFA levels in the serum (the bit of blood that isn't cells) and in the various fat-transport lipoproteins. That stuff's getting everywhere and could be doing lots of bad things.
> Is it that cells built w/ excess PUFAs don't burn energy good and send bad signals?
Could be both. Metabolism is probably borked everywhere because of PUFAs clogging the works just by being the wrong fuel.
And if you're a cell whose metabolism's not working properly then probably everything you do is affected, including, if you're a fat cell, things like generating the appropriate amount of leptin for the amount of fat you contain.
> Brain cells reacting to leptin? Other brain cells?
Again all of that is going to be affected by a metabolism that's not generating enough ATP to power the systems, or enough Krebs-cycle-intermediates to funnel off to actually construct the systems in the first place.
But it could also be that the PUFAs are themselves acting as signalling molecules and interacting with actual receptors, either stimulating them as if they were the real ligands, or binding to the receptors and stopping them working, or binding to the receptors and making them fire too much. Each effect there is going to be complicated in itself, and also exactly the sort of thing that's different from person to person precisely because it's never mattered before. There are hints in the literature that that can happen with leptin receptors.
But there also seem to be direct effects of PUFAs on the activities of various enzymes and pathways. The cancer people seem pretty confident that omega-3 PUFAs act directly on mTOR, the thingy that works out when it's time for a cell to divide, so essentially PUFAs are acting like rapamycin, a natural fungicide that also works on animals and plants. That's terrifying! No wonder the bloody things are "anti-inflammatory". They're paralysing your immune system.
And also at least in liver cells, PUFAs seem to interfere with glycolysis. Again that's going to be a sort of general metabolic derangement that affects everything.
I've done a lot of WOF (water-only-fasting) over the years — up to 10 consecutive days — and I've always regained the weight. Worse, I eventually almost always went above what I weighed initially. I had a strict and controlled refeed of half the length of each fast, but afterwards went on as normal with life. My theories for why I gained back all weight where that 1) I somehow without noticing I ate more than before the fasts, 2) I had lost a significant amount of muscle mass 3) I had lost my eating habits and thus added worse new eating habits, or 4) I had negatively effected my microbiome. The results of your experiment indicate that the first three of these are not very likely. You also recently bashed the microbiome people. So, what's left as an explanation? Set-point theory? — that the fasts were too short to have a lasting effect in the sense that the body remembers and manages to get back to its initial state. I'm still puzzled by this and hope to find an answer some day. Even though everyone says WOF is not a tool for weight loss, we both tried it anyway and confirmed it yet again. So, to repeat myself for anyone reading this: WOF is NOT a good tool for weight loss! Even though I still have a 14 day WOF on my agenda for other reasons than weight loss, I haven't fasted since the pandemic.
> So, what's left as an explanation? Set-point theory? — that the fasts were too short to have a lasting effect in the sense that the body remembers and manages to get back to its initial state
I would argue that this is merely an observation of what apparently happened, not an explanation. Why and how the body "remembers" this would be an explanation :)
My #1 theory is still PUFA settling point. But mostly cause I don't have a better theory.
> My #1 theory is still PUFA settling point. But mostly cause I don't have a better theory.
As in 'blood PUFAs settle to a particular level and that determines lipostat set-point'? That is my theory too, are we starting to agree or are there still differences between us?
I'd also reckon that it's probably adipose PUFA interfering with leptin *production*, but serum PUFA interfering with leptin *reception*.
As in "blood PUFA leads to cell PUFA, and certain (which?) cells containing a certain amount of PUFA burn unclean, or leak electrons, or don't send the correct feedback, or something."
I don't think there's a set point. It's simply a settling point.
Imagine you don't have a thermostat in your house, and it's summer. You open the window to let fresh air in. The house slowly starts to cool until it reaches outside temperature. This is the "normal" condition.
Now imagine you do the same, but somebody has lit a campfire in your house. It might heat your living room by another 10 degrees. As long as he keeps supplying the campfire with new wood, your living room will never reach outside temperature.
If you kick him out and the fire starts dying down, your living room won't immediately reach the outside temperature, and it won't even reach it as fast as in the "normal" situation. But as the campfire slowly starts dying down, the process will return to "normal" closer and closer until the fire is out entirely.
Sure it could absolutely work like that. I think that actually literally is how the temperature of poikilothermic animals works, for instance. They just drift around according to the external temperature, and a lot of the time they're not able to do things because they're too cold.
If you measure their temperature then you get values all over the place, it depends what the environment is doing.
Whereas the homeotherms have their temperature under really precise control, so they can be active whenever necessary.
If you measure their (core) temperature then you'll always get the same value. Even surface temps are pretty stable.
I definitely think that weight works the second way (in all animals). There's an active control mechanism, which is somehow broken in modern people. It manifests as hunger and satiety.
Do you think it works the first way, i.e if you leave people alone with lots of food they'll get fat, or if there's not much food around they'll just get thin without really noticing that they're starving or trying to do anything about it?
I think it's the vast gray area in between of systems that are not under tight control, they just kinda sorta work 85% of the time and the other 15% die cause evolution is a cruel mistress.
Like almost every other system in the body except maybe body temperature. Our light adaptation/sensors are a crude hack, as is our circadian rhytm. Our suffocation/oxygen sensor is a crude hack and we can kill ourselves by huffing & puffing and then going for a dive. Thirst. Sunburn. Pain.
I think if you leave people alone with ad lib food, what happens depends on what the food is. If the food has a metabolic effect like increased appetite, blocking satiety, leaking in the ECT, causing incorrect feedback signals for the cells.. then you might get obesity/anerexia. If not, then probably not in 99% of the people.
Fwiw the microbiome paradigm is working for me. I "reset" it by sticking to a mail order meal plan (instead of mostly Uber eats) for a couple weeks and the difference is pretty large. I recently caved and had one of my favorite junk foods (boneless wings w sour cream ranch) and it no longer tastes good. Like I may as well been eating cardboard. I'm at 1k cal/day and no cravings.
Wings w/ sour cream ranch is just about the most PUFAd food in existence, so yea I could see that sort of stuff nuking your microbiome ;) Chicken is high PUFA, it's deep fried in seed oils, and the ranch is probably 100% soybean oil unless you made it yourself.
Interesting. What types of foods do you get delivered then? How many meals and what macros? 1000 kcal per day seems pretty low; that's lower than what's typically recommended.
I wonder if the fasts are too long and causing damage / unwanted effects of some kind. (Muscle loss? Hormonal changes??) I've been doing one 24 hour fast each week recently, and these seem to be good for fat loss (and hopefully health) and I believe they're short enough to not have any noticeable downsides.
Why do a longer one if a shorter fast is effective and lower risk?
Also your new graph looks great and is very easy to understand. It would be nice to have your whole 2-year history in the same format on the progress page if you're up for it.
New graph? What parts of it? I just painted those fat stripes on the top by hand, if you mean that.
The issue with the 2 year history is that is has way too many experiments. Almost the entire graph is shaded green, and you can't read the labels cause they overlap.
Mmm. I am now quite intrigued. You wrote "One theory is that eating practically 0 fat (like on a fast) forces the body to release more LA, just to get to the very low but existent “essential fatty acid” component."
Well, I have been on a very low fat plan for 10 years now, without having really any oils save for the odd olive oil drizzle here and there. I have a weekly target of 55% complex carbs, 30% protein (lean fish, chicken, egg whites, lentils) and 15% fat and avoiding foods with ingredients not found in home kitchens (highly processed stuff) and eating nothing over 3% fat content. The extreme fat around the liver, which was the spark to start my diet change, is gone -got the contrast scan to prove it-. Maybe I just de-PUFA myself by a different method? I am still not sure why I succeeded and if it is even replicable by others.
Hi and thank you for the comment. Roughly 15 years ago I ended up in an emergency room with just terrible stomach pain. I was diagnosed was extremely fatty liver, high cholesterol, and general inflammation / IBS. I was 202 lbs at 5'10". Some of the symptoms listed looked like hypometabolism but very few.
At first I took satins and was told to "eat less and move more" and got nowhere. After a couple of years of zero progress, I went to a nutritionist. She told me that exercise doesn't do anything for fat loss, but that I should keep moving. She then told me to ditch highly processed foods and eat only food with less than 3% fat. For the next 3.5 years or so, I kept losing weight and fat on a steady but constant decline, I arrived to 135lbs and have stayed there for a decade. The fat around the liver is gone.
Why? I have no idea. It worked for me, and I am thankful for that.
I'm intrigued that you were diagnosed IBS but don't recognise the various hypometabolism symptoms, that's always been on my list of 'things that look like hypothyroidism'.
It is the total sum of the day, and frankly I am usually well under 10%. The 3% rule is based on the label on the product (portion), to give you an example from yesterday:
I had 65 grams of steel cut Oats, but 40 grams is the serving size. So the macros are 44.8g of carbs, 4.3g of fat and 8.7g of protein. Keep adding up those grams over what you eat on the day and the total weight of fat as a % of total eaten gets to between 5 and 10% most days.
Yesterday it was 55% carbs, 7% fats and 38% protein.
I managed to confuse everyone, well done me! My macros are usually around what I described, 55% carbs, say 10-15% fat and the rest protein based mostly on the data from MFP.
Now the "low fat" guidance I took from the nutritionist is to read the label of whatever food I plan to eat, and make sure at the portion level the fat is no more than 3%.
Thus my macros are most days 10% or less fat, and that is the number that is easier to understand. From a food perspective, I care about two things: fat at the portion size should have no more than 3% fat; and avoid any food with ingredients I cannot buy in the grocery store. I hope this helps to clarify what the heck I am doing.
Nice, curious as to your LA number :) Did you get the "Complete?" And I recommend testing first thing in the morning, although with your very low fat diet, the difference might not be that great.
There are some people in your OmegaQuant database who've dropped their LA numbers really fast, do you know anything about what they did? Or is it all just a mirage caused by non-fasting OmegaQuant tests? What happens to those graphs if you delete all the data points which you don't *know* are fasted?
I think many of them are non-fasted tests, but that would probably not explain huge differences. Mine was 2% different and I ate 1,500kcal in mostly SFA between tests. It also likely wouldn't give a uniform, steady drop, that'd be a weird coincidence. It would probably produce more noise in the signal, but both up and down.
I don't know what all those people did, but I think at least 2 experimented with fasting a lot.
It would be so nice if fasting was a magical PUFA-destroying shortcut.... Almost everyone who responded to my little survey had seen marvellous results from being strict about no-PUFAs, but r/saturatedfat is such a weird sample.
In order to get into that list you have to have had bad enough health problems and be curious enough to take the idea seriously, completely overhaul your diet and change all sorts of things as part of doing that, seen good enough results to stick at it, and then stuck around to talk about it.
It could all be noise and reversion to the mean, it could be something else in processed food, it could be something to do with not eating out, it could just be to do with actually paying attention to what you're eating .....
And what am I supposed to make of the big difference between those of us who've gone all out anti-PUFA-lunatic and avoided even things like bacon and olive oil, and those who "just" cut out the 'seed oils'?
I would have guessed that if it's PUFAs, then 'no seed oils' would have done most of the work, but it didn't look like that.
Both Stephen Phinney MD PhD and Eric C. Westman MD - giants in the low carb ketogenic movement - do not encourage intermittent fasting.
Stephen Phinney doesn't want anyone fasting more than 24 hours because after 24 hours, your body starts digging in to your own lean body mass for fuel. Muscles (lean body mass) are so much harder to build up.
While I think that it depends on a lot more how much you can fast until you start burning lean mass, I also haven't had much success with fasting, so I mostly concur.
Hi and thank you for the comment. Roughly 15 years ago I ended up in an emergency room with just terrible stomach pain. I was diagnosed was extremely fatty liver, high cholesterol, and general inflammation / IBS. I was 202 lbs at 5'10". Some of the symptoms listed looked like hypometabolism but very few.
At first I took satins and was told to "eat less and move more" and got nowhere. After a couple of years of zero progress, I went to a nutritionist. She told me that exercise doesn't do anything for fat loss, but that I should keep moving. She then told me to ditch highly processed foods and eat only food with less than 3% fat. For the next 3.5 years or so, I kept losing weight and fat on a steady but constant decline, I arrived to 135lbs and have stayed there for a decade. The fat around the liver is gone.
Why? I have no idea. It worked for me, and I am thankful for that.
I need to do a lot more research on this, but I recall the SaturatedFat folks talking about how fasting can upregulate SCD1, which is implicated in obesity. Makes intuitive sense that going without food would prime the body to try and work extra hard to lay down more fat afterwards.
I've seen a LOT of people (myself included) achieve some stunning results from intermittent/extended fasting. But then again, I started down the path of learning about PUFAs because after a while, even OMAD stopped working to curb the weight gain... seems like it can work well at first, but the body eventually wises up.
The SCD1 thing is one of those things where I'm not sure it's inherently bad, depending on context. For example, I've previously written about 3 people whose OmegaQuants have SIGNIFICANTLY lower LA% (~5%) than even people who've strictly avoided PUFAs for 10 years (who tend to be around 10-11%).
They tend to have much higher de-novo lipogenesis going on, and they also have much increased SCD1. All of them have one thing in common: they are extremely low body fat, even "underweight" sometimes. Some of them also eat extremely low-fat diets.
So in their context it could be fine to have high SCD1 & DNL: if you're very lean you can't get much fat from adipose storage, and especially if you eat a super-low-fat diet on top, the body has to make a lot on its own.
Now a person eating a high-fat diet or having sufficient adipose tissue should NOT have high DNL/SCD1. In that context, it could be pathological.
A fast is, of course, a 0 fat diet. So it could simply mean that the body is responding appropriately by upregulating SCD1.
"Skeptical of the idea that it represents a real lack, cause wtf is in chilies/tomato sauce?"
There are more nutrients than just vitamins and minerals and amino acids! Many other organic acids feed into the Krebs cycle. For example, citric acid, malic acid, acetic acid, etc are all found in foods and are used to produce energy. Tomatoes and peppers both contain citric acid, malic acid, and, well ascorbic acid is vitamin C. But for example, you need vitamin C to make carnitine to be able to shuttle fatty acids to be burned, so craving vitamin C makes sense after a fast because you weren't getting carnitine from meat but your body still had to burn fat, so it was drawing on your vitamin C. And you need plenty of citric acid to make acetyl-CoA, not just for energy production but lots of other functions (reminder that another name for the Krebs cycle is the citric acid cycle). You need malic acid to keep the cycle going, but it comes a few steps before recycling citrate so you may have just used it up that way, though malic acid does other things in the body too.
It is possible to have genetic variants that make it difficult to synthesize or recycle any of those as well, such that you may struggle if you're not eating those foods instead.
You can get an organic acids test (OAT) here: https://truehealthlabs.com/product/organic-acids-urine-test/
I was incredibly low in citrate when I took one a few weeks ago. I think an organic acids test could probably tell you a lot more helpful information about dysregulated metabolic pathways in your body, and maybe a full genome could help you figure out why you seem to need such a specific diet. Sometimes there are things you can do to circumvent genetic inborn errors of metabolism, like simply supplement the thing your body struggles to produce when possible, or supplement larger doses of the cofactors for your goofy-shaped enzyme that doesn't react as easily as it should, so that the chances of it reacting is much higher. For example, I have an ACAD9 problem so that I can't metabolize very long chain fatty acids and have some issues metabolizing long chain fatty acids. That is reflected in my OmegaQuant as well. Because it's involved in assembling complex I of the respiration chain and it is not an issue of producing some other nutrient, but rather difficulty breaking down what is there, my only recourse is to make the enzyme work better. Taking riboflavin makes things pretty functional, and it is *not* an amount of riboflavin I could feasibly get from food (which is typically the case with genetic stuff). I also do better with some carnitine supplementation and glutamine to work around issues with that same gene.
Oh, interesting. That probably makes more sense than my guess, which was "beef has B vitamins."
How did your ACAD9 problem reflect in your OmegaQuant? Super low long chain (18 and up?) fatty acid numbers?
Very high numbers for very long chain fatty acids. They're usually supposed to be a fraction of a percent, but I'll have like three and four times the reference range that are known to cause pathologies, and I get the symptoms of it, too -- like blurry vision is the really obvious one -- if I don't take riboflavin.
The chili/tomato thing is weird, but interesting. I can imagine that you've come to associate tomatoes with protein by eating tomatoes and beef together all the time, (I think when we're in some sort of deficit we tend to crave *the taste that last fixed a similar deficit*) but I'm surprised that your appetite hasn't figured out that tomatoes/chilis alone don't do the trick yet, and focussed itself on getting more beef. Still, if it's usually true that tomatoes/chili come with protein I can see why it might stay confused.
Just in terms of numbers, I've eaten beef w/ tomato sauce about 400-500x the last 2 years, and chilies/tomato sauce w/o any protein maybe... 9 times? So my body could be forgiven in misinterpreting that signal a bit.
I noticed an effect similar to how you describe it a few years after going keto. Before keto, my typical "cravings" foods were pizza and stuff like that. About 1.5-2 years into keto, I started fasting and realized I no longer even craved these carb heavy foods when starving. I was craving steak. Definitely seems like that association is somewhat fluid.
Sounds about right, if your body has got used to 'tomato chili sauce is the taste that fixes protein deficiency' it could take a long time of 'tomatoes without protein' for that connection to get extinguished.
Operant conditioning is pretty well understood and I'm told that those associations can be very difficult to get rid of once they're made.
Still, it's no real problem, and actually a nice association to have. Tomato/chili cravings are your signal for 'I have taken my protein intake (or a specific EAA) too low'. That's a great signal to have, you really don't want to be in actual protein deficit, causes all sorts of trouble.
At that point eat some cheese. And if that makes you stop craving tomatoes (whereas actual tomatoes don't!) then you have an idea what's going on.
My normal tomato sauce has no chilies in it. There is no spicy food in ex150, not even added salt. But chilies and tomato are both weird crack-adjacent New World nightshades I think, so maybe somehow related in my head?
It's possible that chillies taste similar to tomatoes, apart from the capsaicin?
There might be a particular chemical in both that you now think of as the 'taste that fixes tyrosine deficiency', or something?
Yea I'd say they're definitely similar in an acidy/sour way. Another commenter also mentioned how citric acid is an input into the Krebs cycle, necessary to use carnitine or something like that. So could be that not eating beef (=carnitine) increase my requirement for citric acid, and the craving is real.
This post is almost depressing! You did multiple 5 (!) day fasts and still didn't lose weight. Are you getting concerned that you'll ever hit your target weight?
I'm actually so happy at 220ish and feel so great, I'm totally fine with never losing another pound (sustainable, we've seen I can briefly starve myself down lol).
So I wouldn't use the word "concerned." But I sure would like to understand what's causing this "settling point" or "setpoint" or whatever it is.
> I'm actually so happy at 220ish and feel so great, I'm totally fine with never losing another pound.
That's the spirit! Your principal problem is fixed, you're just playing around trying to work out the details now. Well done.
Me too! If a few more other intervention theories don't work, I'm starting to wonder if adding more muscle would help via strength training at this point. Are you in the skinny fat pit? What is your homa-ir (insulin & glucose)? I don't quite remember what your current dexa scan results are too and what BF% you are.
I've seen a few people get to this point where the weight loss stops, but all they do is dieting and maybe cardio at most. I know your doing the X3 bar but maybe focusing on lean mass muscle gain could be the next phase you do to get something moving, and give a long term signal to your body that it's not winter any more, time to wake up for spring.
South asian buff people are probably the best source for getting out of the skinny fat zone since they (epi)genetically have to deal with a lot of crap that makes all weight loss harder and a propensity to be skinny fat.
Also really curious what a genefood test would say at this point what your recommended diet should be. I'm guessing it's probably a very fat heavy one, but I'm also wondering what other details they would bring up.
I'm not skinny fat, I'm muscular-fat (always have been).
My insulin is slightly high, glucose typically very low although in lab draws it tends to be higher (cause I have to walk round a while before the draw?). Typically, at home, I often spend significant parts of the day/week below 70mg/dL right now. Seeing 90 is rare.
Insulin / glucose / HOMA-IR
6.8 98 1.65
10.1 94 2.34
18 88 3.91
10.8 93 2.48
11.8 90 2.62
8.2 92 1.86
8.8 79 1.72
10.4 89 2.29
Well he *did* lose weight, almost certainly some fat even, he just put it back on again. That's to be expected if there's a mechanism trying to keep your fat percentage constant by controlling your appetite.
If that mechanism is broken by PUFAs then the only hope long term is to get the PUFAs out of adipose. You'd think that would take years, but there are people on r/saturatedfat who seem to have done it in a couple of years, I think we should have a careful look at what they did.
I would say fasting isn’t for weight loss; it’s for autophagy, immunity, etc. I’ve fasted (18:6 or 20:4) every day for almost 6 years and I basically never get sick. But it doesn’t cause me to lose weight. My spouse has similar results. Though I'm sure ExFatLoss himself will have had an opposite experience, haha.
Haha I barely consider 16:8 a fast. Just sleep is 8h. If you don't count the cream, I do OMAD. And a lot of the "fasting factors" are not triggered by pure fat (some are), like glucose, insulin (barely), and so on.
It has always been my rule never to smoke when asleep, and never to refrain when awake.
Ah, the Bard.
Really exciting! I'm not surprised that you put the fat back on after fasting, of course, but it's plausible that it caused you to shed more linoleic acid than usual. However I'd also expect that if that had happened it would have brought your set point down slightly and you'd have reckoned the fasting worked. I'm most interested to see how that works out next time you do a test.
Do remember that adipose LA and OmegaQuant LA aren't the same thing. The target might well be 10% OmegaQuant, but it's probably 2% adipose?
If fasting *is* a way of getting LA levels down faster I might have a go myself.
I do wonder whether losing weight and then regaining it brings down adipose LA percentages faster than just staying at a constant weight does. It would be great if it did. You make a good point that when fasting you don't have any LA coming in at all, so you'll have to draw some from adipose for essential needs.
But if I remember rightly it took George Burr's friend six months of an entirely fat-free diet to get his LA from 4% to 2%, and I think that was serum LA (no red blood cells). If that's true then a 2% drop from ten days of fasting seems far too good to be true. (https://theheartattackdiet.substack.com/p/the-george-burr-diet)
In reading your comment, I wonder if it was actually the fast that brought down the OQ LA by 2% or if it was the fact that I basically haven't lost weight in half a year. With 3-4 months of lag in RBCs, maybe it just became "visible" right now, either because of the fast or maybe even a coincidence.
If that's true, my next OQ (already in the mail) should still be pretty low, and I suppose I should then start losing weight again soon? Speaking of predictions.
Yeah, could be, I imagine that losing weight you lose both ordinary fat and PUFA pretty much in proportion, and so the LA percentage stays constant, but if your weight is stable and you're not eating any PUFAs the percentage should come down.
So I can well believe that you've lost a couple of percentage points of LA over the last six months, just like George Burr's friend did on his totally fat free diet.
Unfortunately for ideas about 'PUFA blood levels interfere with homeostat', though, I'd figure that your 'set-point/settling-point/fixed-point/equilibrium' level should have shifted slightly downwards as a result, so you should have already got the benefits. Maybe not much, but it should be there. I can't see why it would lag.
But it's got to be more complicated than that, because everyone who's ever lost weight for any reason seems to report plateaus mixed in with sudden drops, so maybe there's some hysteresis somewhere? Perhaps the actual rate of PUFA release is variable for some reason? Or maybe some receptors somewhere are permanently damaged and need to die off and be replaced to start working again?
At any rate, if 'PUFAs involved in obesity in any way that can be reversed', I'd definitely expect your weight to be going down slowly over time, at least looked at medium-term, as long as you don't change what you're doing. And it doesn't seem to be doing that at the moment, I agree.
I'd be interested to see what happens if you go back to ex150 for a month. I'd predict a weight rise, and then if you go back to ex115 it should come off again. In both cases it should look like an exponential decay I'd imagine, but it would be interesting to see if there were plateaus or if it just happened smoothly.
I'm doing ex150 right now, so your wish will come true and we will find out haha.
Agreed on the "complicated," it really depends on what the mechanism even is. Is it that cells built w/ excess PUFAs don't burn energy good and send bad signals? Then it might depend on which type of cells we're talking about. Brain cells reacting to leptin? Other brain cells? Cells producing leptin? Mitrochondria? Mitochondria of which cells?
It's probably not actually the RBC phospholipids.
> I'm doing ex150 right now, so your wish will come true and we will find out haha.
OK, since I believe that protein is somehow directly involved in this hypothesised set-point-shifting, I will boldly predict that your slight increase in protein intake will lead to a slightly raised set-point, which will result in just enough extra hunger to cause your weight to go up a few pounds, probably in an exponential-decay sort of pattern.
And then if you go back to ex115 afterwards, that will reverse and you'll go back to where you are now. (Or maybe a bit lower because of two more months of PUFA-clearing)
RBC phospholipids themselves are probably not that interesting. RBCs are pretty inert. In mammals they don't even have a nucleus so I don't think there's much going on there at all. They might just be little bags.
Excess PUFAs in the membranes might shorten the lifetime of the cells by oxidising or something, but they might also make them a bit more flexible so they squeeze through capillaries easier and mean the heart doesn't have to work so hard to pump them through a damaged circulatory system.
I'm more interested in the PUFA levels in the serum (the bit of blood that isn't cells) and in the various fat-transport lipoproteins. That stuff's getting everywhere and could be doing lots of bad things.
Agreed, RBC is just an easy to measure proxy. We're the drunk man looking for his linoleic acid under the streetlight.
> Is it that cells built w/ excess PUFAs don't burn energy good and send bad signals?
Could be both. Metabolism is probably borked everywhere because of PUFAs clogging the works just by being the wrong fuel.
And if you're a cell whose metabolism's not working properly then probably everything you do is affected, including, if you're a fat cell, things like generating the appropriate amount of leptin for the amount of fat you contain.
> Brain cells reacting to leptin? Other brain cells?
Again all of that is going to be affected by a metabolism that's not generating enough ATP to power the systems, or enough Krebs-cycle-intermediates to funnel off to actually construct the systems in the first place.
But it could also be that the PUFAs are themselves acting as signalling molecules and interacting with actual receptors, either stimulating them as if they were the real ligands, or binding to the receptors and stopping them working, or binding to the receptors and making them fire too much. Each effect there is going to be complicated in itself, and also exactly the sort of thing that's different from person to person precisely because it's never mattered before. There are hints in the literature that that can happen with leptin receptors.
But there also seem to be direct effects of PUFAs on the activities of various enzymes and pathways. The cancer people seem pretty confident that omega-3 PUFAs act directly on mTOR, the thingy that works out when it's time for a cell to divide, so essentially PUFAs are acting like rapamycin, a natural fungicide that also works on animals and plants. That's terrifying! No wonder the bloody things are "anti-inflammatory". They're paralysing your immune system.
And also at least in liver cells, PUFAs seem to interfere with glycolysis. Again that's going to be a sort of general metabolic derangement that affects everything.
I've done a lot of WOF (water-only-fasting) over the years — up to 10 consecutive days — and I've always regained the weight. Worse, I eventually almost always went above what I weighed initially. I had a strict and controlled refeed of half the length of each fast, but afterwards went on as normal with life. My theories for why I gained back all weight where that 1) I somehow without noticing I ate more than before the fasts, 2) I had lost a significant amount of muscle mass 3) I had lost my eating habits and thus added worse new eating habits, or 4) I had negatively effected my microbiome. The results of your experiment indicate that the first three of these are not very likely. You also recently bashed the microbiome people. So, what's left as an explanation? Set-point theory? — that the fasts were too short to have a lasting effect in the sense that the body remembers and manages to get back to its initial state. I'm still puzzled by this and hope to find an answer some day. Even though everyone says WOF is not a tool for weight loss, we both tried it anyway and confirmed it yet again. So, to repeat myself for anyone reading this: WOF is NOT a good tool for weight loss! Even though I still have a 14 day WOF on my agenda for other reasons than weight loss, I haven't fasted since the pandemic.
> So, what's left as an explanation? Set-point theory? — that the fasts were too short to have a lasting effect in the sense that the body remembers and manages to get back to its initial state
I would argue that this is merely an observation of what apparently happened, not an explanation. Why and how the body "remembers" this would be an explanation :)
My #1 theory is still PUFA settling point. But mostly cause I don't have a better theory.
> My #1 theory is still PUFA settling point. But mostly cause I don't have a better theory.
As in 'blood PUFAs settle to a particular level and that determines lipostat set-point'? That is my theory too, are we starting to agree or are there still differences between us?
I'd also reckon that it's probably adipose PUFA interfering with leptin *production*, but serum PUFA interfering with leptin *reception*.
As in "blood PUFA leads to cell PUFA, and certain (which?) cells containing a certain amount of PUFA burn unclean, or leak electrons, or don't send the correct feedback, or something."
I don't think there's a set point. It's simply a settling point.
Imagine you don't have a thermostat in your house, and it's summer. You open the window to let fresh air in. The house slowly starts to cool until it reaches outside temperature. This is the "normal" condition.
Now imagine you do the same, but somebody has lit a campfire in your house. It might heat your living room by another 10 degrees. As long as he keeps supplying the campfire with new wood, your living room will never reach outside temperature.
If you kick him out and the fire starts dying down, your living room won't immediately reach the outside temperature, and it won't even reach it as fast as in the "normal" situation. But as the campfire slowly starts dying down, the process will return to "normal" closer and closer until the fire is out entirely.
Sure it could absolutely work like that. I think that actually literally is how the temperature of poikilothermic animals works, for instance. They just drift around according to the external temperature, and a lot of the time they're not able to do things because they're too cold.
If you measure their temperature then you get values all over the place, it depends what the environment is doing.
Whereas the homeotherms have their temperature under really precise control, so they can be active whenever necessary.
If you measure their (core) temperature then you'll always get the same value. Even surface temps are pretty stable.
I definitely think that weight works the second way (in all animals). There's an active control mechanism, which is somehow broken in modern people. It manifests as hunger and satiety.
Do you think it works the first way, i.e if you leave people alone with lots of food they'll get fat, or if there's not much food around they'll just get thin without really noticing that they're starving or trying to do anything about it?
I think it's the vast gray area in between of systems that are not under tight control, they just kinda sorta work 85% of the time and the other 15% die cause evolution is a cruel mistress.
Like almost every other system in the body except maybe body temperature. Our light adaptation/sensors are a crude hack, as is our circadian rhytm. Our suffocation/oxygen sensor is a crude hack and we can kill ourselves by huffing & puffing and then going for a dive. Thirst. Sunburn. Pain.
I think if you leave people alone with ad lib food, what happens depends on what the food is. If the food has a metabolic effect like increased appetite, blocking satiety, leaking in the ECT, causing incorrect feedback signals for the cells.. then you might get obesity/anerexia. If not, then probably not in 99% of the people.
Fwiw the microbiome paradigm is working for me. I "reset" it by sticking to a mail order meal plan (instead of mostly Uber eats) for a couple weeks and the difference is pretty large. I recently caved and had one of my favorite junk foods (boneless wings w sour cream ranch) and it no longer tastes good. Like I may as well been eating cardboard. I'm at 1k cal/day and no cravings.
Wings w/ sour cream ranch is just about the most PUFAd food in existence, so yea I could see that sort of stuff nuking your microbiome ;) Chicken is high PUFA, it's deep fried in seed oils, and the ranch is probably 100% soybean oil unless you made it yourself.
Interesting. What types of foods do you get delivered then? How many meals and what macros? 1000 kcal per day seems pretty low; that's lower than what's typically recommended.
I was getting 6 crumble cookies at least once per week if that gives you an idea
That's a lot of soybean oil!
I wonder if the fasts are too long and causing damage / unwanted effects of some kind. (Muscle loss? Hormonal changes??) I've been doing one 24 hour fast each week recently, and these seem to be good for fat loss (and hopefully health) and I believe they're short enough to not have any noticeable downsides.
Why do a longer one if a shorter fast is effective and lower risk?
> Why do a longer one if a shorter fast is effective and lower risk?
If
I didn't lose any muscle, I'd say, after I glycogen'd back up a few days my lean mass (DEXA) was almost back to where it was before.
It could be that the fasting did damage, but I aborted at the first sign of trouble, so hopefully not much if any.
Also your new graph looks great and is very easy to understand. It would be nice to have your whole 2-year history in the same format on the progress page if you're up for it.
New graph? What parts of it? I just painted those fat stripes on the top by hand, if you mean that.
The issue with the 2 year history is that is has way too many experiments. Almost the entire graph is shaded green, and you can't read the labels cause they overlap.
Mmm. I am now quite intrigued. You wrote "One theory is that eating practically 0 fat (like on a fast) forces the body to release more LA, just to get to the very low but existent “essential fatty acid” component."
Well, I have been on a very low fat plan for 10 years now, without having really any oils save for the odd olive oil drizzle here and there. I have a weekly target of 55% complex carbs, 30% protein (lean fish, chicken, egg whites, lentils) and 15% fat and avoiding foods with ingredients not found in home kitchens (highly processed stuff) and eating nothing over 3% fat content. The extreme fat around the liver, which was the spark to start my diet change, is gone -got the contrast scan to prove it-. Maybe I just de-PUFA myself by a different method? I am still not sure why I succeeded and if it is even replicable by others.
Thanks for your posts, and best wishes as always!
Woo hoo, ten years of no PUFAs?
Did any other things clear up? Do you have any health problems left?
Here's a list of 'hypometabolism symptoms':
https://theheartattackdiet.substack.com/p/possible-symptoms-of-hypometabolism
Hi and thank you for the comment. Roughly 15 years ago I ended up in an emergency room with just terrible stomach pain. I was diagnosed was extremely fatty liver, high cholesterol, and general inflammation / IBS. I was 202 lbs at 5'10". Some of the symptoms listed looked like hypometabolism but very few.
At first I took satins and was told to "eat less and move more" and got nowhere. After a couple of years of zero progress, I went to a nutritionist. She told me that exercise doesn't do anything for fat loss, but that I should keep moving. She then told me to ditch highly processed foods and eat only food with less than 3% fat. For the next 3.5 years or so, I kept losing weight and fat on a steady but constant decline, I arrived to 135lbs and have stayed there for a decade. The fat around the liver is gone.
Why? I have no idea. It worked for me, and I am thankful for that.
Amazing! BMI 29 down to 19.
I'm intrigued that you were diagnosed IBS but don't recognise the various hypometabolism symptoms, that's always been on my list of 'things that look like hypothyroidism'.
How do you get 15% fat in your diet if you don't eat anything that contains more than 3% fat?
It is the total sum of the day, and frankly I am usually well under 10%. The 3% rule is based on the label on the product (portion), to give you an example from yesterday:
I had 65 grams of steel cut Oats, but 40 grams is the serving size. So the macros are 44.8g of carbs, 4.3g of fat and 8.7g of protein. Keep adding up those grams over what you eat on the day and the total weight of fat as a % of total eaten gets to between 5 and 10% most days.
Yesterday it was 55% carbs, 7% fats and 38% protein.
So your oats were roughly 6% fat (4.3/65)? How does that square with nothing over 3%?
I managed to confuse everyone, well done me! My macros are usually around what I described, 55% carbs, say 10-15% fat and the rest protein based mostly on the data from MFP.
Now the "low fat" guidance I took from the nutritionist is to read the label of whatever food I plan to eat, and make sure at the portion level the fat is no more than 3%.
Thus my macros are most days 10% or less fat, and that is the number that is easier to understand. From a food perspective, I care about two things: fat at the portion size should have no more than 3% fat; and avoid any food with ingredients I cannot buy in the grocery store. I hope this helps to clarify what the heck I am doing.
By portion size you mean by weight? So, 3% fat by weight which due to the 5/9kcal thing is around 10% by carolies?
https://foods.exfatloss.com/food/2343973
15% kcal from fat in oats, intriguingly also 14% from protein haha. Oats are a high-protein diet. The fat is 33% LA.
Well if you ate <=3% fat, you would've very likely dePUFA'd yourself. Even if you only ate pure soybean oil, 3% isn't very much :)
Have you done a fasted OmegaQuant Complete to check your linoleic acid levels? They're $100 on Amazon.
Do they ship them to Canada? I will check!
Just bought direct from their website. They had a promo code but $15 shipping to Canada.
Nice, curious as to your LA number :) Did you get the "Complete?" And I recommend testing first thing in the morning, although with your very low fat diet, the difference might not be that great.
Got the complete, will share the results and follow your advice. You owe me $130 Canadian Monopoly Money, LOL.
$130! And I thought our inflation was bad.
There are some people in your OmegaQuant database who've dropped their LA numbers really fast, do you know anything about what they did? Or is it all just a mirage caused by non-fasting OmegaQuant tests? What happens to those graphs if you delete all the data points which you don't *know* are fasted?
I think many of them are non-fasted tests, but that would probably not explain huge differences. Mine was 2% different and I ate 1,500kcal in mostly SFA between tests. It also likely wouldn't give a uniform, steady drop, that'd be a weird coincidence. It would probably produce more noise in the signal, but both up and down.
I don't know what all those people did, but I think at least 2 experimented with fasting a lot.
It would be so nice if fasting was a magical PUFA-destroying shortcut.... Almost everyone who responded to my little survey had seen marvellous results from being strict about no-PUFAs, but r/saturatedfat is such a weird sample.
In order to get into that list you have to have had bad enough health problems and be curious enough to take the idea seriously, completely overhaul your diet and change all sorts of things as part of doing that, seen good enough results to stick at it, and then stuck around to talk about it.
It could all be noise and reversion to the mean, it could be something else in processed food, it could be something to do with not eating out, it could just be to do with actually paying attention to what you're eating .....
And what am I supposed to make of the big difference between those of us who've gone all out anti-PUFA-lunatic and avoided even things like bacon and olive oil, and those who "just" cut out the 'seed oils'?
I would have guessed that if it's PUFAs, then 'no seed oils' would have done most of the work, but it didn't look like that.
I've read that chicken is actually the #1 PUFA source in the US. Bacon probably not far behind.
So cutting out the seed oils probably only cuts out a fraction of the seed oils, as you found out with peanut butter.
Both Stephen Phinney MD PhD and Eric C. Westman MD - giants in the low carb ketogenic movement - do not encourage intermittent fasting.
Stephen Phinney doesn't want anyone fasting more than 24 hours because after 24 hours, your body starts digging in to your own lean body mass for fuel. Muscles (lean body mass) are so much harder to build up.
While I think that it depends on a lot more how much you can fast until you start burning lean mass, I also haven't had much success with fasting, so I mostly concur.
Hi and thank you for the comment. Roughly 15 years ago I ended up in an emergency room with just terrible stomach pain. I was diagnosed was extremely fatty liver, high cholesterol, and general inflammation / IBS. I was 202 lbs at 5'10". Some of the symptoms listed looked like hypometabolism but very few.
At first I took satins and was told to "eat less and move more" and got nowhere. After a couple of years of zero progress, I went to a nutritionist. She told me that exercise doesn't do anything for fat loss, but that I should keep moving. She then told me to ditch highly processed foods and eat only food with less than 3% fat. For the next 3.5 years or so, I kept losing weight and fat on a steady but constant decline, I arrived to 135lbs and have stayed there for a decade. The fat around the liver is gone.
Why? I have no idea. It worked for me, and I am thankful for that.
That's great, congrats! Sounds a lot like the McDougall starch diet?
I need to do a lot more research on this, but I recall the SaturatedFat folks talking about how fasting can upregulate SCD1, which is implicated in obesity. Makes intuitive sense that going without food would prime the body to try and work extra hard to lay down more fat afterwards.
I've seen a LOT of people (myself included) achieve some stunning results from intermittent/extended fasting. But then again, I started down the path of learning about PUFAs because after a while, even OMAD stopped working to curb the weight gain... seems like it can work well at first, but the body eventually wises up.
The SCD1 thing is one of those things where I'm not sure it's inherently bad, depending on context. For example, I've previously written about 3 people whose OmegaQuants have SIGNIFICANTLY lower LA% (~5%) than even people who've strictly avoided PUFAs for 10 years (who tend to be around 10-11%).
They tend to have much higher de-novo lipogenesis going on, and they also have much increased SCD1. All of them have one thing in common: they are extremely low body fat, even "underweight" sometimes. Some of them also eat extremely low-fat diets.
So in their context it could be fine to have high SCD1 & DNL: if you're very lean you can't get much fat from adipose storage, and especially if you eat a super-low-fat diet on top, the body has to make a lot on its own.
Now a person eating a high-fat diet or having sufficient adipose tissue should NOT have high DNL/SCD1. In that context, it could be pathological.
A fast is, of course, a 0 fat diet. So it could simply mean that the body is responding appropriately by upregulating SCD1.