Recent research mentioned in a Discover magazine article shows that our fat cells live for about 10 years. I guess this could mean that if you diet off extra weight, and maintain that loss for years, then the fat cells that were once bloated with fat will die off, making it easier to maintain. Maybe.



Link

You mean, I could finally have thin thighs at 80?? I'd better get to work.

This is a fascinating article. Thanks for posting the link.

As opposed to living for hours or day or weeks or months like most of our OTHER cells.

It figures.

PJ

Unlikely. Fat tissue grown through what's called insulin-induced lipohypertrophy (fat lumps due to injecting insulin in the same spot for years) stays grown. Fat tissue grows like that through the action of insulin, specifically chronic hyperinsulinemia, in a process called pre-adipocyte proliferation and differentiation. But fat cells aren't the only cells that compose fat tissue as illustrated by a recent drug PTP1 which acts on blood vessels, killing those blood vessels, thereby shutting down oxygen supply to adjoining fat cells which then kill themselves (or just die of asphyxia) and release their content permanently and ultimately reduce overall fat tissue mass locally. This effect occurs only in apparently recently grown new fat tissue likely through this same mechanism insulin-induced lipohypertrophy, i.e. they found the drug has no effect on the lean. As far as I'm aware, there's no innate mechanism like that.

It doesn't just happen with fat tissue, but also with other tissues like the pelvis which is grown wider during pregnancy, and does not return to its original size after birth. More than that, if I'm not mistaken, each subsequent pregnancy goes through this same growth process even if the pelvis has grown wide enough already, though maybe not as much as the first time.

The way I see it is that there's no evolutionary incentive to return tissues to previous small size even if the conditions that prompted these tissues to grow bigger do not exist anymore, and we have only a set number of stem cells that eventually run out. Consider muscles. They grow bigger, and the blood vessels that supply them grow more intricate and extensive. When muscles grow smaller due to negative pressures like lower testosterone or starvation, the blood vessels remain intricate and extensive anyway, indicating that there's no reduction in the number of cells that make up muscles, only a reduction in the protein that forms the mechanical component of muscles. The idea is economy. No reason to kill off more cells than necessary when growth conditions are still there, no reason to kill off more cells than necessary when these same conditions don't exist anymore. The alternative is that once grown, more cells are needed to replace them, and if destroyed, even more cells are needed to replace those in case of subsequent growth. Better to stick with existing growth and only replace those as needed, exactly like it's done in normal conditions where tissues remain the same size. Or put differently, there's no reason to kill off perfectly healthy cells just because it's an elegant idea.

Well, that's just my opinion. I mean, oh how I wish I saw it differently, but my brain gets in the way.

Well done, Martin. Although I could see an evolutionary argument for dismantling a supporting network for blood vessels that aren't currently needed. The resources required to maintain the network might be more metabolically expensive after some period of time than tearing down that network and rebuilding it when needed again.

Fat tissue, OTOH, is so important as an energy reserve that it makes sense to maintain it for a long time.

Yeah... they jump from whether starvation just depletes fat cells, or kills them, to whether you can stick to a "healthy regimen" long enough. Is that a healthy regimen of starvation?

If starvation or semi-starvation doesn't stick, or comes and goes, what do you get? Maybe a growth promoting stressor, in starvation. When you push muscles to their limits, when you challenge brain or bone, what happens? It grows, increases connectivity, becomes denser, makes the appropriate adaptations. What's the appropriate adaptation to a starvation challenge? Getting fatter, so the next bout of starvation will be less life-threatening?

A few years ago, Turtle posted another study in female mice, reducing their food intake to 95 percent of controls made the mice fatter. I always wished they'd had a control for the restricted arm of the study, where mice were restricted to 100 percent. I think all you can eat is probably less stressful than all you could have eaten, the control mice didn't have that much more food, but they had the option to eat much more if they'd wanted. If a wild mouse can only just barely get the amount it wants to eat--maybe that's a signal that even harder times might be coming, and it had better become metabolically stingy. Of course this works with chow, probably doesn't work with a Chinese food buffet.

In the Minnesota Starvation study, when the men regained their weight, lean mass didn't return to it's original levels until after the fat mass had surpassed its original levels.

http://www.ncbi.nlm.nih.gov/pubmed/19602538



Maybe a warning here for any form of weight-loss-however adipoctyes are depleted, whether by starvation or ketogenic diet, returning to a high carbohydrate diet might be risky--the weight loss might predispose to an increase not just in fat storage, but also an increase in adipocyte number. This might explain anecdotal evidence that a low carb diet doesn't always work as well the second or third time around. The role of insulin in fat storage doesn't change, but fat cell structure might.

Playing devil's advocate--by being low in protein, and very low in fat, it's possible that something like the potato hack or the Rice diet approaches this from another angle--they might provide nutrition with a low-anabolic potential, not just for muscle tissue, but for fat tissue as well, carbohydrate, protein and fat could all be individually rate limiting for cell proliferation.

Teaser, I don't even remember that post. Got the link?

http://forum.lowcarber.org/showthread.php?t=408410

Had to google it... thought maybe I'd remembered wrong.

Improved link, from end of other thread (thanks Turtle2003)

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880162/

Concerning the apparent premise of the original article that a person's fat cells will die off in about ten years (leaving them skinny? ) doesn't the body just replace most cells that die off? Otherwise how would anyone ever grow to be over ten years old if all their fat cells died off in ten years? I'm pretty sure my body's figured out some way to replace those little guys because I'm still fat.

I think the theory is that supposedly, as you get fat, your body produces more and more fat cells, and they are stretched to a large size due to your extra weight. If you lose the extra pounds and maintain that lower weight, your body has no need for those extra fat cells. As your fat cells die off, they will be replaced, but with not as many as when you were at your highest weight. You will still have fat cells of course, just not as many as you had when you were obese. Your body would hopefully wind up with only as many fat cells as you had when you were slimmer.

Yeah, that's the theory. But there's got to be some reason for those fat cells to die off besides an idea. There's got to be some purpose, some mechanism, like when they grow more numerous, but the other way round. So is there such a mechanism? I forget exactly but in another study, they found that fat cells react to physical pressure like when they grow too large and get all bunched up together, and then the effect is new fat cells. Maybe the pressure signals pre-adipocytes. Now what if there was an opposite mechanism when fat cells shrink too small, i.e. negative pressure stimulus? With insulin-induced lipohypertrophy, we'd need an opposite of that, so lack of insulin just like with diabetes type 1. Would that do it? Bear in mind that it's not just fat cells that need to die off but also blood vessels and maybe nervous cells too. The idea here is that all cells have a purpose and this purpose must be removed for cells to be removed.

Here's an interesting mechanism. In an experiment (I read it years ago on another forum) with a sort of cufflinks, they blocked off circulation at key points, and this stimulated local muscle growth independently of mechanical stimuli like lifting weights. In fact, just light weights caused significant muscle growth so the stimulus would be something like lack of oxygen or something else in the blood. Imagine exertion to a point where you're really out of breath but you keep pulling that rope. Muscles grow bigger to compensate. Of course, I doubt this growth occurs at this very moment, but the stimulus causes subsequent growth and the next time exertion is not so quick to occur, you can pull the rope a little longer a little harder. Now ironically the opposite of this stimulus is surplus, too much oxygen too much blood going to muscles. Do muscles just shrink to compensate now? Maybe they stop growing because the previous stimulus is gone, but that's not a reversal of growth.

How about the mechanism that kills off almost half the brain cells during a certain period in infant growth? I'm a little vague on this phenomenon, but it's an idea and maybe it occurs at other times but perhaps not as dramatically.

I guess the point is that the idea should be supported by at least some biological/physiological plausibility.

It just occurred to me that if we see cell lifespan as a function of workload or stress, then fat cells must have it real easy, right? Well, if we return the body to good health, then fat cells would have it even easier now, and there'd be even less reason for them to suicide.

I don't know if I'm remembering this properly but there was an article on fat cells and the death of

Fat cells are long-lived but they do die. That, in fact, their longevity is programmed by body cycles of famine, i.e., if famine occurs approximately every 5-7 years, fat cells will live at least eight to 10 years or something like that to ensure it doesn't get caught short of stored fat when a famin arrives...even if it arrives a little later than expected.

Diet cycles stand in as famine cycles.

Fat cells multiply but don't shrink; they fill with water to keep them available for refilling during the next feast/pre-famine period as the energy needed to maintain them fat less is less than that needed to create new.

Water filled fat cells will refill with fat in preference to expending energy in preparation for the next famine.

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I remember when I found/read this article, it made a lot of sense to me.

So...
Fat cells dying and releasing contained water is what creates the "whoosh" of weight loss.

It explained plateaus.

It explained weight spriraling and the period before weight regain when it seemed like you were off the diet but not gaining weight for a while.

It explained why you really shouldn't restrict calories too much.. i.e., it mimics famine and leads to fat cell longevity and easy weight regain.

It explained why people could be turtles and/or never get the Atkins energy surge.

MartinLevac said;



That reminds me of the stuff on angiogenesis. That's the proliferation of blood cells. A few years ago somebody posted some stuff here on the effect of blocking angiogenesis on fat cells--this is a way to really starve them out, no blood supply, no growth, fat cells die and aren't replaced. They use the same idea against cancer sometimes. That makes me wonder if blocking circulation to a muscle, and then giving it a stimulus that would normally increase blood flow to the muscle, but blocking the blood flow, works in part because it causes the stressed muscle to secrete more blood vessel growth factors--and then increased blood flow to the muscle helps to increase growth. The signal for the muscle to do this might be lack of oxygen. Maybe that's one of the reasons glycolytic exercise increases muscle size in the first place, glucose is burned because oxygen can't be delivered to the muscle fast enough to support maximal effort, so blood supply is expanded to better support fat metabolism.