The oddity is the blip downwards of weight in canola fed rats, highlighted by the red oval on the graph:
which needs to be read in conjunction with the food intakes in this graph, also highlighted by a red oval:
I've copied the food intake graph and laid it over the weight graph to make it a bit clearer:
Because the red graph is in grams of food I've annotated the important energy intakes next to the related data points. Obviously the switch from chow to high fat diet (fine orange line) massively alters the caloric intake despite the weight eaten being the same on the day before and after the switch.
Interminable aside: if any paper gives you the caloric density of any food used you are assured that the group are idiots, even if they are very, very clever idiots. They believe you can fool a rat's hypothalamus in to over-consuming calories by increasing the caloric density of the food. Or fool it in to under-consuming calories by diluting them down with sawdust or the equivalent (usually cellulose). As if evolution is that gullible. Do not, under any circumstances, accept any of such a group's ideas about satiety, food intake or bodyweight. Ever. End aside.
Anyhoo. On day one the high fat fed rats increased their energy intake from around 227kJ (55kcal) to 355kJ (85kcal), a rise of ~56%. I find this impressive and in the same league as the Schwartz lab rats on D12492, who increased their caloric intake by ~87% on day one in this venerable graph:
In Protons terms the canola oil fed rats still used 227kJ for running their metabolism but "lost" 128kJ in to their adipocytes via the enhanced insulin signalling of linoleic acid (LA) and alpha linolenic acid (ALA) due to their low F:N ratios. The rats needed 227kJ, they lost 128kJ so needed to replace those 128kJ, therefore they ate 227+128 = 355kJ. They stopped at 355kJ because that's when they stopped being hungry. Overall weight did not change because 227kJ of chow weighs the same as 355kJ of the canola oil diet (Hmmm, chance or pilot study????). 128kJ is about 3g of fat gain.
Simple.
What happened next is much more exciting. On day two of the canola oil diet the rats weren't hungry. They only ate 155kJ that day. The weight of food eaten dropped by ~13g, and so did the weight (~10g) of the rats, food is heavy, they ate less, they weighed less. But they still needed those 227kJ to run their metabolism. They ate until they weren't hungry, that's what they do. Why weren't they hungry?
They must have accessed the full 227kJ that they needed, otherwise they would still have been hungry. They obtained the missing 72kJ from their adipocytes. Without "trying", without being hungry. Remember, they always eat to satiety.
The logical explanation is that there was an acute drop in insulin signalling in their adipocytes which released 72kJ worth of FFAs, which meant that there was no need to eat the 72kJ's worth of food needed to reach the full 227kJ to run metabolism. 72kJ is the energy available from about 2g of fat.
From the Protons perspective acute loss of insulin signalling is a standard effect of reduced mitochondrial membrane potential caused by uncoupling. PUFA uncouple. At high intakes this over rides the obesogenic effect of their reduced F:N ratio.
The blip of weight down then back up again mostly reflects food weights with a lesser contribution from adipose weights, but the latter adipose changes are the factor responsible for the hunger changes which drive the food intake changes.
Uncoupling explains the blip. The only thing which surprised me was how rapidly the effect kicked in. I would have expected that about a week would be about the time scale but here it was 48h. Those are the data. I have to revise my views in the light of it. You don't often get given a gift-horse (of daily food intakes and daily body weight changes) to consider examining the mouth of!
The following day the rats increased their food intake. Under steady growth the rats still needed the standard 227kJ/d plus some extra for uncoupling losses. Adipocyte size does not continue to shrink because the uncoupling using biological uncoupling proteins is ATP dependent, low intra mitochondrial ATP reduces the effectiveness of uncoupling proteins. This is distinctly different from chemical uncoupling to which there is no upper limit and so these can give extreme weight loss or even death.
The rats still needed 227kJ/d for metabolism and 62kJ/d for uncoupling, hence 289kJ/d. This happened pretty consistently throughout the rest of the high fat period. They stayed slim but not too slim. Despite eating around 20% extra in calories compared to the chow fed mice.
Peter
There is another very strange/interesting feature on the food intake graph. I'll see when I can find time to describe it.
Interesting as always. It looks like AMPK activation (ACC phosphorylation) after switch to canola, definitely not activated by butter. Could 13% of ALA be that effective? I think it can, acetate and ACSS2 as in many cases before :-)
ReplyDeleteBtw, additional released fat cannot be burned without ACC phosphorylation.
Jaromir
First, we might want to point out that the name "Canola" was a rebranding of rapeseed oil so people would think it was safe.
ReplyDeleteThe uncoupling is part of what I've been thinking about lately - is the cause of much of obesity the lack of uncoupling - some environmental effect that make us run cooler than we should when there is an abundance of energy available?
I've talked to countless people that complain of cold intolerance when they are trying to diet. T3 drops with fasting.
https://www.sciencedirect.com/science/article/pii/S001457930300320X
As usual, there is a pretty good list of confounding control loops that effect coupling - as well as fusion and fission of MT.
Peter, couldn't find if the diet contained sugar. If yes, then it would explain LPS poisoning with butter diet, and also lactate as MCT1 transporter activator for acetate effect acceleration.
ReplyDeleteJaromir
Sticking this here sort of randomly. I started to read your blog, got a bit confuzzled, and went back to 2007 (not time travel, just clicking/scrolling). So now I'm back. Tried to post a couple of comments, but they never appeared. Maybe a different browser will do the trick. Anyway, I'm hoping this will be a useful anecdote.
ReplyDeleteOkay. First: I'm not anhedonic. (Simpler to say I'm hedonic, I guess?) Or I don't think I am. But I did try the "carbosis" thing. Or, more accurately, I'm 1.5 weeks in.
Background: 56yo, low carb for 20+ years, carnivore for 4. Pretty much always in ketosis. However, it does squat for weight loss--I fast a lot. Feel pretty good, but I tend to be about 50 pounds heavier than when I was 18. Used to run a lot, stopped when I got heavy and busy. Still have my 45ish resting heart rate, blood pressure still good, no health issues.
First recent discovery came from a random comment by my sister that she can't lose weight unless she exercises--which she followed by saying she had read enough that she really didn't understand why it would be true (she is also a low carb person). So I theorized about leptin resistance possibly being affected by exercise, checked pubmed, and ended up signing up to run a marathon in March--this being my excuse to actually take time to go run, or run/walk anyway, which I actually love doing for its own sake. I lost 30 pounds in two months with no dietary changes. However, I was about 30 pounds over my typical weight when I started. (Got busy with work, didn't mess around with fasting). I did also stop eating chicken and American pork. Hadn't really worried about fat types previously. (Paul Mason's comments about phytosterols made sense to me & I thought ancient Egypt's metabolic syndrome issues were a strong argument against linoleic acid per se being the main issue--I did stop eating all seed oils a decade ago, though.)
more below....
Then I found Brad Marshall's stuff via your blog, and tried the croissant diet. Gave up after a week and a half--basically I lost my nerve after regaining 15 pounds, all of it seeming to be in my belly. Went back to what I was doing & lost the weight again in about 3 weeks. Some of it being water, I'm aware. But I do wonder about glycogen vs inflammation. I was concerned bc it seemed to me that the perpetually elevated FFAs might lead to full-body insulin resistance. I also wondered about rats with shredded abs & whether their muscles were larger, weight being the same, because of intramuscular triglycerides. No idea if that's the case, but it was a concern.
ReplyDeleteOkay. Carbosis, the fun way. Cans of wild caught salmon, 500 calories, 10 grams of fat. Tuna, much lower in fat, if I get hungry for protein. Lots of french fries, or chips I guess, except they're really french bakes. Sliced potato, rolled in egg white, seasoned, baked. Sometimes with white flour. Bread made with Guinness and honey and the only fat from a single egg from a friend's free-range bug-eating chickens. Rice. Salsa. Salmon, rice, and salsa are combined, then eaten in a sandwich or an egg white wrap. I've been drinking beer with meals, which is nice. Also I've consumed a couple of sodas for the fun of it. They weren't very tasty though.
No caloric restriction, been doing this a week and a half, down just under two pounds. I went way up on the first couple of days, then have been losing steadily since. Will that continue? No idea.
I don't feel as good/energetic as I do whilst wallowing in carnivory. But I don't feel unhealthy either. My body temperature, which had been trending slowly upward for the last few months, instantly normalized.
No idea whether the weight loss will continue. I doubt I'll gain much, though. Previously I'd just decided that I probably had tons of little hungry adipocytes...but I didn't care enough about potentially present hyperplasia to try to do anything about it beyond the regular fasting (often eating every other day, usually 2 meals on a feeding day). I don't mind the fasting at this point, you know? It's nice in its own way.
But anyway. The carbosis thing is 'cause I was thinking about stearic & palmitic acid supplementation in a zero-carb scenario. Tried it, via sausages (so the casings would contain the fat). It seemed to be helping the weight come off, and amused me when I drove my temperature north of 100 degrees F.
OTOH Brad Marshall's diet was supplementing in the context of high insulin. I figured there was a good chance of increased SCD1, thus not quite storing/burning the fats I'd prefer.
I've also got this notion of fasting but with stearic acid chocolate bars. I made a few...Irish butter & stearic acid in about equal proportion, plus cocoa powder & spices/stevia. They're tasty, they raise my body temperature, and they might or might not increase FFA flux, thus hurrying along the process of dumping linoleic acid from adipocytes. I mean...maybe. It's an idea. I've tried doing this, but only for about 3 days. Seemed pretty easy, but the carbosis idea strikes me as funnier.
Okay. Maybe that'll show up? Either way, if you see this, THANK YOU for your thoughts/blog. It's been a fun ride.
Oh yeah. About the leptin thing. I found an interesting paper that showed leptin decreasing after exercise--but only after, I think, about 12 hours had passed. And either that paper or another one showed leptin decrease only after fasted exercise. Of course anything written about leptin is going to be filled with weird analyses...but anyway, I discovered that I would max out my breath ketone meter--not right after exercise (acetone ppm goes down every time, which I find interesting) but for the following two mornings I max the little gadget out at 99ppm. I have no idea whether leptin-inspired uncoupling is involved, or some completely separate process, but the exercise (generally 2-3 hours of running/walking, repeated every three to four days) definitely did very cool things to weight loss.
ReplyDeleteAlso! I forgot to mention above that I find myself in mild ketosis (4ppm) every morning while eating the carbosis diet. Makes sense to me--tons of palmitate around after the sugar goes away. But it's neat to see. My take on all of this: I can either eat more saturated fat, or make my own out of junk. Burns the same either way, maybe.
I promise I'm done now. {8'> Thanks again though.
Hi Jaromir, yes, AMPK activation is important. But you have to distinguish between uncoupling suppressing insulin signalling and the effect of that reduced insulin signalling on AMPK activation, insulin being a direct suppressor of AMPK in addition to AMPK being a suppressor of insulin signalling. As karl says, feedback loops within feedback loops. BTW MCT don’t uncouple, pretty well not at all. So butter has no lever against the loss of calories in to storage by MCTs. Oleat is a moderate uncoupler but palmitic acid is the worst, cf PUFA.
ReplyDeleteOh, they diluted the 5075 with butter or canola oil so the sugar content will always be less than the control group but exactly how much less is now buried in the mists of antiquity and the limited disclosure of information (unless it helps you support the narrative).
David, there is a pattern to my blogging. I blog and I think. Sometimes the thinking takes a long time (this current paper has been on my radar for months). Under these conditions I neglect Hyperlipid. When I finally get back to actually writing there are often many, many comments and it would take weeks to go through them all. So I tend not to, which is a fault but I’m not a perfectionist. My bad.
I’ll spend a little time reading your comments and will reply here.
BTW, if moderation is turned off for the comments they just fill up with viagra spam!
Peter
Clarification: MCTs don't uncouple *directly*. FGF21 is another factor. Higher level signalling....
ReplyDeleteInteresting David. I have gravitated to carbosis being pretty much a near zero LA diet. But carbosis with sugar, especially in large amounts, will also actively push the liver to release FGF21 and cause thermogenesis and active fat oxidation.
ReplyDeletehttps://pubmed.ncbi.nlm.nih.gov/28886439/
I also do have a paper somewhere where isolated liver tissue (IIRC isolated guinea pig liver slices) is ketogenic if exposed to fructose. Not gone through the details but might also be relevant.
Best
Peter
Thanks, Peter. But...you are a very dangerous man.
ReplyDeleteOf course it's not your fault. You don't know me. But your comment about "sugar, especially in large amounts" inspired me, as it was always destined to do, worlds without end, amen. I can see it now! I'll call it the "hummingbird diet," unless that name's actually taken, but it's okay if I don't Google it. Running around in my neighbors' backyards, guzzling from the hummingbird feeders...at this point of course I must accept that the red dye they use will also turn out to be somewhat beneficial. Or will at least stain my teeth, adding a bit of humor to the police reports.
This is even better than my speculations earlier about how a croissant diet might potentially lead me to appeal to a particular subset of cannibals who would find great value in a "high oleic, highly marbled" carcass. Sadly, this idea didn't seem practical, as I wasn't able to target this market segment on Facebook with ads, & I don't want to mess around learning another platform.
Slightly more seriously, I've got a few weeks to play with. I'll try avoiding sucrose (and, sadly, also the beer...I have no idea what the mechanism might be behind this increased FGF21 level, so for all I know alcohol might also be relevant combined with maltose/glucose?). Then I'll try consuming a lot of sucrose. Not planning to do any of this carbosis stuff past Thanksgiving, 'cause it's amusing but I doubt it's anything close to optimal.
Thanks yet again. And I wasn't complaining about the previous unpublished comments, exactly. Just letting you know...anyway, as I kept reading I found most, possibly all, of the answers/responses to my questions/speculations in either later posts or comments. I think the most recent post to which I'd submitted a comment was from something like 2009. At any rate, no great loss.
Hmm. "Animals that consume fermenting fruit and nectar are at risk of exposure to ethanol and the detrimental effects of inebriation. In this report, we show that the hormone FGF21, which is strongly induced by ethanol in murine and human liver, stimulates arousal from intoxication without changing ethanol catabolism"
ReplyDeletehttps://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00041-4
Going to have to read more.
Also I'll dial the protein back even farther, just as a stunt. Seems to be relevant.
ReplyDeleteSeems like a potential explanation for the "alcohol causes weight gain at low/moderate levels of consumption but weight loss at high levels" notion I've run into. Might not be the higher alcohol consumption per se but the replacement of protein that's relevant? FWIW, bourbon added to my zero carb eating has reliably increased weight gain for years. Which is a shame.
I suppose there's not much chance of fatty liver in the midst of carbosis, especially starting from years of ketosis. So what the heck, fructose and alcohol will be consumed...after I try avoiding them for a bit, anyway.
Off to work. Thanks yet again.
Oh. One more one more thing. Seems to me FGF21 would preferentially target visceral fat, if the noradrenergic bit is real (I haven't read enough to know anything yet; just speculating). Kinda wonder what happens after visceral fat is significantly decreased. Probably something.
ReplyDelete"FGF21 mediates the recovery from alcohol intoxication by directly activating noradrenergic neurons in mice"
https://pmc.ncbi.nlm.nih.gov/articles/PMC7053867/
FGF21 looks like a surrogate for hepatocyte caloric overload. Alcohol, fructose, MCTs all seem to do it. All you have to avoid is locking those calories in to hepatocyte lipid droplets using enhanced insulin signalling via PUFA, aka fatty liver...
ReplyDeleteSo this is interesting, at least to me. I stopped consuming fructose and alcohol. Gained 1.2 pounds back the first day, and .6 pounds the second. Which is consistent with my previously-consistent "I gain weight no matter what I eat, unless I also fast" experience. But not consistent with what I've experienced recently. I really want to find lots more ways to use the word "consistent" atm, but I recognize this urge is not helpful. Still, though....
ReplyDeleteStill in ketosis both mornings, though 2ppm and 3 ppm instead of my previously-consistent 4ppm. (FWIW, AFAICT I'm in ketosis every morning, no matter what I eat--though on a zero-carb diet with exercise, I max out the meter at 99ppm, whereas if actually fasting, but without exercise, I get something more like 45-60ppm even 11 days in--which I've only done twice, but it's surprisingly easy...for whatever reason, at that point my body decides, or has so decided thus far, that I'm going to eat, so I do. Meaning that I have become very very hungry, which didn't happen previously.)
But. No, of course I have no idea how accurate my breath ketone meter might be. Though it does give very close results with repeated tests, and also varies strongly between myself & wife & kids in a manner apparently consistent with diet and exercise. So I figure it's at least directionally valid. And yeah, I only eliminated fructose and alcohol for two days. I'm choosing to regard this as significant...enough for me to change my ways and see what happens, rather than continue as I've been doing for the last couple of days, anyway.
I wonder, now, about FGF21 and the oft-repeated story of impaired alcohol resistance on a low carb or keto diet. Could it be because dietary protein inhibits FGF21 even though ketosis/starvation upregulate it? Maybe. Lots of maybes. But why should alcohol on an empty stomach be more intoxicating? Is thatt even a real thing, though, or just an oft-repeated bit of noise? I have no idea. Though I've always wondered why, given that people generally have to pay for drinks, and they're drinking to experience the effects of alcohol, they wouldn't prefer to get more bang for their bucks by failing to eat? And, while I'm on the topic, the practice of paying for and consuming sugary "cocktails" seems as if it might be very much in the best interest of the establishment selling these items. Not only are the non-alcohol ingredients likely inexpensive, but the sugar involved might actually improve alcohol tolerance & encourage more purchases? I really don't know. I don't like sweet drinks. Even beer, which until recently I'd avoided for years, is only tolerable if very very hoppy. But I'm curious.
Anyway, I am going to re-add fructose and alcohol to see what happens.
Also, an emotionally disturbed but consistently entertaining friend of mine, about 30 years ago, added sugar to his Coca-Cola and consumed very little else for a while. I didn't weigh him, but he seemed to lose something like 50 pounds very quickly. At the time I figured it was all about calories, and he somehow wasn't consuming very many. But the math for that just doesn't work out. I acknowledge that life is full of math problems & we want to quantify the effects of variables when we don't actually know either the value of constants or even which is which. But I now suspect something interesting was going on.
ReplyDeleteAnother also. I have read, and could chase down the studies, I guess, but it's only parenthetically interesting so I'm not going to, that switching from sugary drinks to diet drinks does not induce weight loss. I'd figured that it might matter a bit if drinking previously-sweetened beverages from a bottle or can, but matter not at all if using sweetener packets helpfully labeled "no calories!" whilst containing dextrose/maltodextrin (doesn't count as "sugar" on a label, apparently, though it's clearly just glucose in one form or another). But. What if fructose is actually, in the absence of linoleic acid, a weight-loss drug? Hmm.
ReplyDeletehttps://pubmed.ncbi.nlm.nih.gov/21621801/
ReplyDeleteWeight loss greater in moderate fructose diet than low fructose, both being energy-restricted
It's an RCT, so interesting. There are probably better studies out there that might disprove the notion. I'll probably look for 'em at some point (and perhaps read more than the abstract from this one as well), but right now I need to get actual work done.
Fructose is a weight loss drug at high dose rates. But you need enough to get adipocyte exposure high enough to induce adipocyte insulin resistance, or you need to keep it to the liver at low levels to reduce systemic insulin penetration. There is a sweet spot between the two which might make it obesogenic but I'm somewhat doubtful...
ReplyDeleteBTW there may be problems from fructose separate to bodyweight weight adjustment of course. I'll hold fire on that one.
P
Hi Peter, do you have any reference to insulin as direct suppressor of AMPK? I see this effect as not direct and mechanistically I suppose, it works through fructose-1,6-bisphosphate (FBP), the most important glycolytic metabolite. Insulin should lead to more glycolytic ATP and elevated cytosolic NADH should control GAPDH. This is good control of insulin resistance. Elevated NADH elevates FBP and trigger fat synthesis by suppressing AMPK, which elevates PPP and NADPH production, for fat synthesis. Perfect mechanism. If this is not possible, H2O2 starts to control GAPDH and blocks it. Then uncoupling cannot activate GAPDH again. Uncoupling needs NADH aspartate-malate shuttle working properly to control GAPDH. It's H2O2 that controls uncoupling via UCP by separating fats from membrane phospholipids, but too much H2O2 blocks GAPDH and deactivates AMPK, more robust protection against H2O2 overload than uncoupling, but fat making, permanently. This also leads to histone deacetylation and normoxic HIF1 activation via ACC. References are on my blog.
ReplyDeleteJaromir
Thanks yet again, Peter. Weight loss has restarted, though I'm just barely under my weight previous to the weight gain when stopping fructose/alcohol, so who knows what'll happen there. It'd be nice, at some point, to have a stable weight--any stable weight might be fine.
ReplyDeleteIn the context of carbosis, thus reduced insulin in general, at least post-prandially relative to what carbohydrates might normally cause the pancreas to generate, I wonder if fructose might be especially slimming without much regard to adipocyte insulin resistance. I guess a person could order up some gel capsules and fructose powder and find out. Or drink soft drinks. Which taste horrible. Think I'll just continue to have a beer with my meals, though, and force myself to drink the occasional soda. Even bourbon cannot make them taste good, sadly. Morning body temperature is up to 98.3, and of course higher later in the day. I'm still curious about this little experiment, and I've managed to make the food taste pretty good, but I am looking forward to returning to zero carb. I just can't run or recover as well this way, and it irritates me.
Thinking about what I wrote earlier. I wonder whether my fasting insulin is also reduced, since my morning blood glucose has gone from 90-95ish to 75-80ish, even starting from years of zero carb. In my head this makes sense, as I should be getting a higher palmitate percentage due to semi-LIFO release from adipocytes, especially with SCD1 not so much in play as in a typical diet...at any rate, I'm thinking in terms of higher full-body insulin resistance, which might--maybe--mean the liver is simply releasing less glucose, as my muscles won't be using it. Or of course I could suspect that glucose is lower due to increased insulin, but I doubt things would work out that way. Something has definitely reduced fasting glucose, anyway. Resting heart rate is also down, which surprised me.
I suppose it's also possible that higher insulin resistance in muscles means my reduced exercise capacity is 'cause they used to run on more sugar than I thought they did. It'd be interesting, if true. I had thought myself to be thoroughly fat-adapted by this point. But, you know, maybe not?
ReplyDeleteAbout that RHR thing. In general, and I have no idea why this would be the case, my HR gets to its lowest point when I'm sitting around in the morning, drinking coffee. All of a sudden it's actually going down to similar levels while I sleep, even lower actually than ever before, and staying at about the same level when I drink the coffee. Maybe down slightly, 1 or 2 bpm, but not the 4-7 bpm it used to drop vs sleeping levels (it's amazing just how much mostly useless info a Garmin watch will provide). I've tried to chase down a dropping pulse with caffeine, but couldn't find any results. At any rate, I'm around 40-41bpm lately instead of 43-46. No idea why carbosis would do this.
ReplyDeleteThere's a start here Jaromir. It's an idea I like but I've not donme the deep dive from my perspective
ReplyDeletehttps://pubmed.ncbi.nlm.nih.gov/24487023/
https://pubmed.ncbi.nlm.nih.gov/25172224/
Peter
About that FGF21 thing & carbosis. First off, "Fibroblast growth factor 21 regulates energy metabolism by activating the AMPK–SIRT1–PGC-1α pathway" (https://www.pnas.org/doi/10.1073/pnas.1006962107 ) interests me. But it also confuses me, as does everything else I read about FGF21. However, it is apparently at least somewhat increased in both ketosis and outright fasting. And, depending on which paper I read, it may be increased by exercise. And, on the topic of ketosis, I did find--somewhere or other--a paper that showed rats who had previously adapted to a ketogenic diet could re-enter ketosis independently of liver glycogen status. I'm not a rat, but ketosis is pretty common for me, so this might partially or fully explain the "some degree of ketosis every morning regardless of diet" results I get.
ReplyDeleteWhich, along with some related thoughts mainly having to do with the potential downsides of multiple hyperglycemic episodes in the same day in a state of carbosis and minimal post-prandial insulin, plus concerns about ensuring the liver has time to deplete itself of fat "stores", plus wondering if enhancing overnight ketosis would be helpful, has me wondering about the following plan to (maybe?) maximize weight-loss efficacy without fasting or much risk of metabolic stumbling blocks:
0. Moderate run/walk, probably for an hour or so, while fasted. Post-coffee in my case--it's a performace drug, and I like it. Possibly, at least sometimes, some upper body resistance exercise as well. Confession: this is how I like to spend my mornings anyway.
1. First meal: lots of carbohydrate, very low protein and fat. Add fructose/alcohol depending on tolerance and whim.
2. Second meal (optional): zero carbohydrate, low-ish fat, higher in protein. This exists only, in my head, as a means to introduce lean red meat, likely calf liver, in moderation. As it would be followed by another very low fat meal, any "second meal effect" caused by enterocyte fat storage/release ought to be minimal for the next day's carb-fest/breakfast. Alcohol is optional.
3. Third (or second/last) meal: zero carbohydrate, very low fat (unsaturated; stress on omega-3 options). Alcohol is optional.
(continued)
ReplyDeleteI'd noticed that forcing myself to drink 3 sodas with high fructose corn syrup raised my oral temperature to 99.5 for several hours, and I woke up still at 98.7. So there appears to be a fairly long-lasting effect of...something...even though FGF21 supposedly has a fairly short half life. Also, I had a horrible ravenous hunger all night & slept badly. No cravings, just physical hunger. Feasting on carbs the next day did not help much even with a very full belly, but a zero-carb (still low fat) later meal resolved it...and on the morning after the zero-carb second meal I noticed greater fat loss than expected. In general I've been gravitating toward one meal a day, but delaying the protein might or might not increase FGF21. Also, if I just really wan't hungry later, that first meal might suffice.
Completely anecdotal stuff, and I could be way off base about everything. Just wondering if anyone has any thoughts...also, any additional metabolic levers I might hit would be interesting. I'm actually quite pleased with my weight loss thus far--still planning a return to zero carb, but I'm quite interested in this general approach to therapeutic nutrition. I was really hoping for weight-stability at best. Kind of expected lowered fasting glucose, didn't expect lowered heart rate or general satisfaction...even my exercise performance, while initially disappointing, seemed to respond well to a zero-carb high protein second meal.
I also have a notion, if I got to some weight that I thought would be nice to maintain, of combining stearic acid in chocolate-bar form with CLA while otherwise fasting, maybe for a few days at a time. Maybe to induce a bit of adipocyte apoptosis? Eat food for a while, rinse, repeat? Wouldn't want to go too far down that route, and I'd be lucky to find CLA supplements with the correct form of CLA, but at fairly low doses it might work. The not-helpful CLA would probably (maybe) be no worse than regular-type LA, and a few grams a day shouldn't affect much. Again, maybe.
IOW I've never been diagnosed as diabetic, but am quite sure I've experienced metabolic syndrome. And, for nearly 20 years, nothing but fasting has reduced my weight...I'm tired of having to think about it. If zero carb worked on its own, I'd be fine. But it doesn't. I think I can fix it, though. I'm gonna, or know the reason why.
ReplyDeleteHa. Or, if not the reason, at least I'll know what I did and what happened. (Though all this is with the caveat that I do understand that simply reducing LA exposure, whilst cursing my previous love of smoked pork belly, possibly whilst also eating some cold-water fish--I like fish--might eventually work on its own. But I like seeing results in the near term, and I'm fairly accustomed to doing things other folks might see as extreme--by which I mean all the fasting--so this is just more-but-easier of the same.)
{8'>
Never mind; experiment terminated. Had my very first migraine. Very cool visual effects--I wondered at first whether I'd somehow detached my retina. But both eyes? Anyway, looked like somebody was about to tear a hole in the space-time continuum, or come through from the Nevernever, or some such thing. Pain afterward, and visual symptoms went away. No idea whether it was diet-related, of course, but I'm done. Back to meat, meat, and a side of meat. Not much of a hardship....
ReplyDeleteI had meant to include this earlier, from "Metabolic switching is impaired by aging and facilitated by ketosis independent of glycogen", https://pmc.ncbi.nlm.nih.gov/articles/PMC7244089/
ReplyDelete"Keto-adaptation does not rely on glycogen depletion. (A) Glycogen levels in the liver while fasted or fed in young and aged rats on the SD or KD. SD-fed aged rats were not able to maintain liver glycogen when fasted, whereas KD-fed aged rats were. (B) Muscle glycogen while fasted or fed in young and aged rats on the SD or KD did not change across age, diet or feeding status groups. (C) Young SD-fed rats had significantly higher liver glycogen than all aged rats and KD-fed young rats during the first 3 days of the diet, but levels were similar in all groups on day 7 and beyond. (D) The GKI did not correlate with the amount of glycogen in the liver during keto-adaptation for young animals on the SD or KD. (E) The GKI did not correlate with the amount of glycogen in the liver during keto-adaptation for aged animals on the KD, but did significantly negatively correlate during this time period in SD-fed rats. Data are represented as group mean ± 1 SEM. In panels A-B: TRF standard diet n = 14 young, n = 15 aged; TRF ketogenic diet n = 14 young, n = 15 aged. For panels C-E: n = 20 per group for all groups."
Obviously this is rats, not humans. But shouldn't this be even more true of us? Inside my skull is a strong suspicion that it's the case. Anyway, it's always struck me as unlikely that a carnivore would be unable to maintain/use glycogen stores--also that exercise performance would therefore suffer. Once a person is out of the post-prandial higher-insulin period, why not go into ketosis? I noticed it happening in myself, and it makes sense in my head at least, but I may be an outlier? Or not?