this post was submitted on 07 Jul 2025
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https://pubmed.ncbi.nlm.nih.gov/29991030/
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.
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
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/
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
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.
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!
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).
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).