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And all the antivaxxers I ever knew sure like recreational substances too. (lemmy.world)
submitted 1 year ago by to c/memes@lemmy.world
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[–] 6 points 1 year ago (18 children)

You’re basically blaming the drug for the person’s inability to psychologically deal with diet.

No, I don't. I'm just stating facts on how the human body works. With extreme willpower you might be able to counter this for a time, yes. But it will be a serious uphill battle, and the messenger chemicals from the depleted fat cells do not just stop because you will them to. You will just have to live in a state of perpetual raving hunger then. The few who can successfully overcome this for a significant time are rare, indeed.

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  • [–] 3 points 1 year ago (17 children)

    I’m down 100lbs and been chilling there for a a while actually. (I do bulk/cut cycles of around 30lbs for bodybuilding so my total weight loss fluctuates from like 120lbs to 90lbs depending on how that’s going. Just for disclosure)

    But I’ve heard a few people mention this idea that “fat cells stick around forever” and “send hunger signals to fill you back up”. Do we have a scientific source for this?

    My other thing with it is like, that’s not the reason someone gets fat the first time right? Because the idea is your fat cells start multiplying after a certain weight? So regardless it still seems important to address that first cause and not repeat it

    But for me personally I just haven’t really experienced it at all lol. I’ve found that actually the type of food I eat makes me hungry and more likely to go off track. Like any fast food, most prepackaged snacks and prepared meals from the grocery store.

    Like I could eat an 800cal pint of ice cream then have dinner 45 minutes later. But 200 calories of frozen grapes and I’m like, stuffed lol. Or I’ve also noticed if I have a doughnut in the morning (work offers them) I’m hungry all day, but eggs cheese oats and yogurt leave me satisfied to the point where I’m not hungry at all when I get home, and eat just because I know I need the nutrition from dinner.

    Anyway sorry for rambling, really I’m just curious to get to the bottom of the “depleted fat cell” thing. I had never heard of it the entire time I was losing weight/maintaining then all of the sudden I’m hearing it pop up in lots of places, even lemmy now

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  • [–] 2 points 1 year ago (7 children)

    https://pubmed.ncbi.nlm.nih.gov/29991030/

    In adults, fat cell number is constant over time in spite of a large turnover (about 10% of the fat cells per year) when body weight is stable. A decrease in body weight only changes fat cell size (becoming smaller), whereas an increase in body weight causes elevation of both fat cell size and number in adults.

    https://pmc.ncbi.nlm.nih.gov/articles/PMC4371661/

    This one's not as easy for me to quote.

    Basically the gist of the whole idea is that your body maintains the level of fat cells pretty steadily as an adult. When you gain or lose weight the cells just grow or shrink, but they can only grow so big before you need new cells to store more energy and your body will build them. Each of the fat cells have a part to play in signaling that you're in a deficit and need to consume more calories (when we didn't have such calorie dense foods readily available this was probably correct most of the time). So, if you have 2 or 3 times the number of fat cells then you "should" that's increasing the signaling you receive to eat, making it harder not to (simplifying that a lot). In normal maintenance, your body still maintains that turnover pretty steadily so it generally doesn't go away.

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  • [–] 2 points 1 year ago (6 children)

    I’ve read the first study already, it doesn’t comment at all on the hunger signaling aspect.

    The second study is just proposing this as a mechanism which may account for weight regain. They spin off pretty quickly into a more matter-of-fact tone while presenting the hypothesis itself, but at the moment it remains speculation. I obviously haven’t had the time to click through to every reference in there, but so far the links I have checked similarly lead to speculation.

    Basically I think it’s somewhat dishonest to present this hypothesis as a statement of fact. I feel like the inevitable result of this mischaracterization will cause people to not even try. Why bother if something is probably impossible, or only one in a million could do it?

    Thank you for linking it however, and I will be very interested to know if Professor MacLean verifies the concept. Of note, in the conclusion they propose that environmental and behavioral interventions will be important for combatting this effect, if it does turn out to be true

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  • [–] 1 point 1 year ago (5 children)

    You're right the second article probably doesn't support the hunger bit enough. As i understand it, the hunger signaling is largely an absence of leptin, which is a hormone that regulates appetite. The increase in fat cells from obesity leads to more leptin production and then leptin resistance, so it's less effective. When you diet and lose the weight the fat cells aren't producing as much leptin and you're resistant to what they are producing so you're comparatively hungrier than you may have been if you stayed at a healthier weight. I believe the leptin sensitivity can recover and be improved through other ways but I'm not an expert.

    https://pmc.ncbi.nlm.nih.gov/articles/PMC6354688/

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  • [–] 2 points 1 year ago (4 children)

    Thank you again for the link, but it seems like you’re just reiterating the hypothesis without any supporting evidence? We have a proposed mechanistic explanation for the phenomena that requires further study. My point of contention is that it should be presented as such, and not as a granted fact

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  • [–] 1 point 1 year ago (3 children)

    Maybe my sources aren't great, I use kagi nowadays over Google and they have an academic filter (like Google scholar). That's all I used to find the few things I linked.

    It's well established that your fat cell count is relatively stable as an adult and that as you gain significant weight that your body creates more fat cells to store this energy. It's known that the number of cells stay relatively stable even after losing weight, they just shrink. It's also known that leptin, or lack there of, affects your hunger. These things specifically are well documented. Other points of what I shared, and the overall impact may be, still hypothetical.

    I'm not going to keep looking for and reading articles because I'm not finding what you're looking for and that's all good. I don't want to act like I'm an expert, I'm just a nerd reading things on the internet.

    That's not to say, though, that this fat cell count is the end all be all and it's impossible to lose weight because you've already gained too much — your own situation is proof of that. It's just added context, not a barrier. Highly satiating foods like what you've mentioned, grapes over ice cream, eggs oats and yogurt over donuts, these make a much bigger impact on your overall hunger. I feel it too, I'm overweight and working on losing it, and if i snack on something like chips, it almost feels like it does nothing for me. That's why all the weight loss advice mentions high protein and High fiber foods.

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  • [–] 2 points 1 year ago (2 children)

    Gotcha, yeah and thanks once again for the discussion. What I’m looking for basically is just evidence for the claim posted above us, specifically that “it is a fact that weight loss results in lifelong ravenous hunger due to fat cell signaling”

    Scientists all the time come out with reviews and proposals that ultimately fizzle out without supporting evidence. So before I am able to believe any specific claims I need to see that it’s an actual scientific finding rather than just something tentative that has caught headlines (like I said, it happens all the time).

    Since you like reading studies in general, for your own amusement I would suggest investigating the claim “cooking rice with coconut oil, then leaving it in the fridge overnight, will reduce the calories absorbed by your body by half!”

    It’s a total and blatant piece of misinformation based on a chain of bad news reports made about a study that claimed something totally different, and was subsequently never confirmed. Yet I have met people in real life who swore by the method (even though they struggled to lose weight regardless of this supposed calorie cutting “hack”).

    The weight loss space in general is totally flooded with this type of misinfo which is why I get so particular about it. Thank you again!

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  • [–] 1 point 1 year ago

    That reminds me of that peanut butter, professor nutz. They claim that due to adding certain fibers to their peanut butter, it reduces the digested calories from around 200 calories to 36 calories. They took a concept that exists, fiber-fat bonding, and an in house pilot study of 6 people over 2 weeks, and use that to market this as some kind of miracle peanut butter. Is it technically possible that somebody eating that peanut butter only digests 36 calories per serving? Yes, but it's (to me) very unlikely and changes person to person (which they admit).

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  • [–] 1 point 1 year ago

    What I’m looking for basically is just evidence for the claim posted above us, specifically that “it is a fact that weight loss results in lifelong ravenous hunger due to fat cell signaling”

    In my reading the the literature there is nothing to support this "fat cells make you hungry" theory.

    At best there is an association between fat people and fat cell population, but given hyperplasia is more common in people of european descent its not a causal connection. Plus this theory doesn't account for fat people from hypertrophic populations (asians).

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  • [–] 2 points 1 year ago

    Because hunger has to do with vitamin balancing and a lot of people don't get enough of certain vitamins which keeps them always behind.

    Eg vitamin A makes your skin slough off in excess and can kill you in very high doses. To treat high vitamin a in the ER, doctors use vitamin e. Vitamin E can make you bleed in excess if you have a deficiency of vitamin K, so vitamin e excess is treated with vitamin k. Vitamin e deficiency can also cause blood clots. Vitamin D interacts with all of the above as well and they actually all interact with each other and make uo a large part of the immune system with downstream effects on other vitamins including b vitamins.

    For a lot of people, once they understand how to balance their vitamins, they dont feel hungry anymore. But people alwyas want a magic pill that splves everything instead

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  • [–] 1 point 1 year ago (7 children)

    The "fat cells are multiplying" is normal when having surplus calories in the body. The "empty fat cells scream hunger" is something that was suspected basically for ages, but has finally be proven not long ago, the paper is less than half a year old. It had been referred to here on Lemmy, at least to a science or nature article that pointed to the paper.

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  • [–] 3 points 1 year ago (6 children)

    Could you direct me to the paper where it was proven? There seems to be a notable amount of bad journalism and broad misrepresentation of the science on this topic.

    We are basically discussing whether or not obesity is an inescapable condemnation, so we should not sensationalize the topic whatsoever, and we should especially not present it as a fact if it is not a fact

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  • [–] 1 point 1 year ago (1 child)

    Could you direct me to the paper where it was proven?

    Sadly, no. I sat down and tried to remember the title, but it won't come up. It is not old, two to three months at most, I'd say. I'm going to bed now, maybe it will pop up tomorrow. In that case, I'll update this.

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  • [–] 1 point 1 year ago (2 children)

    Found it. It was older than I thought, though: https://www.nature.com/articles/s41586-024-08165-7

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  • [–] 1 point 1 year ago

    To be honest, reading thru the study and poking at some of the discussions about it online, it seems to not be remotely saying what people are saying it’s saying lol.

    Like they weren’t able to find many of the results they expected in actual human samples compared to the mice. They also found that slower weight loss seemed to correspond with fewer and less severe epigenetic changes.

    That second point there was never really expanded on beyond a throwaway statement, but it jumped out at me because the humans studied received bariatric surgery. Which causes massive weight loss very quickly. They even cited that as a potential confounding variable.

    It’s also not really about “fat cells multiplying” at all, but rather how a collection of dozens of different factors differ between never obese and formerly obese samples, and only at the two year mark after a weight loss intervention.

    Their own conclusion is that “they have not proven” their findings have anything to do with weight regain. This is then bizarrely and immediately followed by what can only be described as an unprompted advertisement for Ozempic, along with speculative musing that further study is needed to determine if it could be used to “erase or diminish” the epigenetic memory (despite semaglutide being unrelated to the experiments and appearing nowhere else in the paper?). Interestingly enough, there’s also an extant conflict of interest statement linking one of the researches to several pharmaceutical companies, including Novo Nordisk

    All in all, it strikes me as nothing more than yet another case of bad science reporting. With people kind of going in with preconceived notions, glossing over all of the details, and emerging with snippets taken out of context (body remembers being fat! It changes your genetics!). Lo and behold all the online discussion centers around just the provocative headline and the speculative sections of the paper.

    It seems like the researches even deliberately tried to use language to bait this type of response from the general public (although this is now just speculation on my part). In summary, I am unpersuaded by the available evidence. Thank you however for linking it! There is a lot of other interesting info in there

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