Considering that it's the carbs that control fat tissue, low carb allows the lowest homeostasis without starving. If we have to cut calories to drop that point lower, then we're semi-starving and we can't do that for the rest of our lives and maintain health. So if we've got a bigger fat tissue, we either go with low carb and accept that's it for that, or we go with other ways to actually physically reduce fat tissue.

After all is said here, I can conclude that we regain not because we're weak-willed, but because we've been starving ourselves to grow leaner. So as soon as we start to eat a normal amount of food again, the new homeostasis is restored. That is, the new homeostasis that was created by the years of a high carb diet. This new homeostasis is not just more fat in fat cells, it's more fat cells.

One thing though--how a person goes low calorie might be a factor. For all we know, cutting back to 1500 calories, then 1200, then 800, slowly getting lower and lower might be much worse than doing a 2 or 3 week, 500-calorie diet, and then a period of maintenance, and then another course of dieting. What's more stressful? 500 calories for 30 days, or 1200 calories or so with no end in sight? Sometimes more stress, short term, isn't all that bad a thing, all sorts of positive metabolic adaptations favouring lipolysis etc. might take place.

I'm right on the low-carb bandwagon. And I don't doubt that straight calorie restriction can be a pretty crappy weight loss tool sometimes. My own personal experience with calorie restriction prior to going low carb was pretty cruddy. I just think it belongs in the toolbox. That isn't to say that everybody should use it. Sort of like IF, some people thrive on it, some people's tolerance for skipping meals is just awful. Atkins called a low-calorie diet a "second-best" diet, compared to low carbohydrate. Now that IF has caught on, maybe it gets a demotion to third-best.

Martin, the reason I'm bringing up this stuff about tweaking low carb when weight loss stalls in a thread about the excess proliferation of fat cells is that we can't assume that further weight loss is impossible due to a sort of generalized lipohypertrophy until we've either exhausted the toolbox (tried anything reasonable that might work, been tested for thyroid, hypoglycemia, etc) or actually had a sample of our fat tissue examined in a lab or something.

We don't know that our body fat will rise to the same level if we eat less and then return to an ad-lib low carbohydrate diet. This may be true, but we can't assume that it's true. This may be our experience with returning to a high-carb diet after restricting calories. Is it the same if the maintenance diet is low carb?

NancyLC said;



Nancy, I get that and I've read Pounds and Inches. When I said



I meant to say "the diet was effective for weight-loss," I wasn't referring to the other claims made for hcg, I'm fairly agnostic about those. I just don't know--but I see lots of people online who are pretty happy that they went on hcg, and with good reason.

Lipodystrophy due to injecting insulin in the same spot for years is real. The effect of insulin of fat tissue growth is real. Do you believe that injecting insulin and secreting insulin has a different effect on fat tissue growth? I don't. I believe insulin has the same effect regardless of where it comes from. Just like I believe every other hormone has the same effect regardless of where they come from.

Remember what Taubes said? Carbohydrate drive insulin drive excess fat accumulation. Combined with the evidence about lipodystrophy due to injecting insulin in the same spot for years, this is what we get:

Carbohydrate drive insulin drive excess fat tissue growth in size and quantity.

If you really think we should not assume that's what happened, then why don't you propose an alternative.

Do I believe localized hyperinsulinism at an injection site is different from secreted insulin? Yes. That insulin will have different effects on fat tissue growth with the one than with the other? I don't dispute that either of these can cause fattening, one locally, one general.



And I haven't disputed that a generalized increase in numbers of fat cells might occur, it's well established that some overweight or obese people simply have a greater number of fat cells. Insulin isn't the only hormonal factor in this, but it's certainly a necessary one.



Here's an alternative; not assuming. Not making assumptions until you're sure what's going on on an individual level.

I think this is an interesting avenue of exploration. Although what one is really doing in that case may be much more to tweak the hormonal status than to enjoy the benefits of the reduced calories during the shock diet.

(Even my stubborn situation can re-set - I know because I've seen it; confoundingly odd though... it was after way, way too much dental anesthetic ... with epinephrine ... and feeling sick for a couple days from it ... that I started losing about a pound every other day for 15 lbs., and stayed at that lower weight several months, and then it trended right back up, slowly. So whatever that shock was on my system certainly helped for awhile.)

On an individual basis. OK, I agree. But what does that mean? Does it mean that insulin works differently for every one of us? Or does it mean that insulin works the same way in everybody, but the difference is in how much insulin we secreted over how long, and thus how much fat tissue we've grown?

Insulin works the same way in everybody. It works the same way in every species. Inject insulin in a dog, it grows fatter. In a mouse, a monkey, in humans, they grow fatter. There is no reason to believe insulin will work differently in some humans.

Insulin won't maybe cause an increase in fat tissue. It will cause an increase in fat tissue. That's what insulin does. Lipodystrophy due to injecting insulin in the same spot for years is inevitable. Just like the different fat distribution in men and women is inevitable. It's inevitable because that's the nature of these hormones: That's what they do. They change our physiology, and they change it in very specific ways. Insulin's way is to grow fat tissue.

The only assumption I'm making is that insulin does its job, and does it well. You want me to assume that maybe insulin didn't do its job this time around. Consider how much sense that idea makes.

You believe injecting insulin and secreting insulin are different. In what way are they different? Injecting will grow fat tissue, but secreting won't? Or injecting will grow fat tissue more, and secreting will grow fat tissue less?

Insulin is not the only factor in fat tissue growth, I agree. But it's the primary factor. We don't inject massive doses of T3 or adrenaline or IGF-1. We don't secrete massive quantities of T3 or adrenaline or IGF-1. We inject massive doses of insulin, we secrete massive quantities of insulin. That's because we eat massive amounts of carbs. and because insulin is the only thing that takes care of the carbs we eat.

Taubes said epinephrine is opposite insulin in the hormones that control fat tissue. That explains partly why you lost weight. Another reason might be that since you were losing weight due to epinephrine, you had more fuel available, and were smaller, so you were less hungry, so ate less, so secreted less insulin to cover that food which in turn allowed even more fat to be released from fat cells. But once you reached stable weight, you stopped releasing surplus fat from fat cells, so had less fuel available, so were more hungry, so ate more, so secreted more insulin to cover that food, so stored just that much more fat in fat cells, so ate a bit more to compensate, etc until homeostasis was restored just that little bit higher.

^yeah except for the ate-more part (didn't); I did definitely feel more energy during this weight loss, like moribund resources were being freed up ... and while that didn't mean overt exercise at a different level than before for me, it probably did mean more spring-in-the-step throughout the day and just a higher burn rate. (Maybe at plateau time it's the case that instead of prompting me to eat more my body simply powers down to energy-conservation status.)

Instead of there being changes in caloric intake over this time, I wonder about (in my case and generally plenty of others as well) the hormonal change when weight loss is under way. I do take thyroid hormone and at 15 pounds lighter, my usual dose felt like too much ... and it's often the case that as weight decreases thyroid doses need to as well, although it can be tricky and isn't the only thing affecting weight loss by any stretch. (On a thyroid forum I visit plenty of people experience weight gain when their dose is too low of course, but also when it's too high.)

I'm not saying that thyroid was the only hormonal change involved, but in general I suspect there were several hormonal levers at work - and no doubt feedback loops.

But like you alluded to, I think the epinephrine shock was probably the key that unlocked that weight-loss phase. Coming soon: the epi-pen diet!

To try to bring this back to the main topic of the thread - fat lumps - I can tell you a couple things about an opposing action to that localized insulin-related fat gain ... decades back while having a scar repaired a medical tech injected a small amount of local anesthetic that was supposed to have been diluted by a factor of 10 or something but wasn't ... I was fine but did end up with a dent from localized fat loss along the injection site. There was epinephrine in that I believe, although several things will cause localized fat loss including I believe local anesthetic by itself (consider the -caine source), and of course steroids injected for pain relief etc., and tangentially I am told that smokers have a hard time hanging onto fat that has been transferred from another part of the body (like to fill out dents along the lines of the aforementioned) ... also I'm told by a surgeon that smokers' fat looks different - is more yellow - than nonsmokers'. All that generally, to me, speaks to what are probably opposite actions to insulin. (The epinephrine and -caines, certainly, but the steroids and tobacco components perhaps in a roundabout way.)

Bodybuilders have known about epinephrine for a while. Nicotine also acts on fat tissue although indirectly, as Taubes points out in GCBC. You're right, there are many factors at play.

This thread got me thinking:
http://forum.lowcarber.org/showthread.php?t=424497

Cayenne powder anyone?

Meant to add in the above that cell death probably plays a partial role. (Doubt that's all of it.)

Ha. By the way if you make dark chocolate ice cream ... The kind using cream and several egg yolks ... you can stuff about 5 inescapable the recommended cayenne in it without it being very hot, when making hot chilie chocolate ice cream. (Needless to say use noncaloric sweetener.) Made the regular version ... with the extra cayenne ... as a party gift and it was a big hit.

OK, sorry to have the trifecta of posts in a row here (!) but this is an interesting link that gets into some of Taubes' views on insulin resistance in fat cells via nicotine.

http://www.why-low-carb-diets-work....eight-loss.html

That's a good website. I refer to it all the time. I just realized that there's this confusion about what obesity really is and this website doesn't escape it. To illustrate:

Ever since I made up my mind about lipodystrophy/-hypertrophy, I can't help but make the clear distinction between fat, and fat tissue. Consequently, this explanation of what must be done to reduce fat tissue permanently just doesn't make sense anymore. We can't reduce fat tissue permanently just by releasing more fat than we store. This balance is controlled by hormones, and if hormones are back in balance after going low carb for a while, then whatever the size of fat tissue will dictate how much fat we'll end up with. The bigger the fat tissue, the more fat we'll end up with. And what dictates how much fat tissue we have is how much insulin we've secreted for how many years, just like with local lipohypertrophy due to injecting insulin in the same spot for years.

So, a more appropriate explanation of what we must do to reduce fat tissue permanently is to do something that will actually reduce fat tissue, not just the amount of fat it contains.

And, since releasing more fat than we store merely changes the amount of fat that fat tissue contains and not the size of fat tissue itself, and since eating normally after having starved ourselves will make us regain, we have to keep doing whatever we're doing to keep this abnormal balance intact. Because there is no doubt about it, this is utterly abnormal if we have to keep starving ourselves to maintain this weight.

This is the case for liposuction. Albeit just removing several pounds is considered massive lipo ... it is no way to remove poundage even in the double-digits, rather for contouring and spot treatment. (Still, wonder about the hormonal effect of slight reductions.)

Also in the model you mentioned, with fat cells (AKA tissue), I'm not convinced the issue was ever just removing the fat from them; to what extent do fat cells vary in their percent of water content? (It's been alluded to here and elsewhere that as weight is lost the body may go through a period of introducing more water to the fat cell before dropping pounds. Is there ever a situation in which that water, if this happens, is retained and the body won't let go of it?) Water is heavy.

Every time I heard somebody talking about water replacing fat in fat cells, it was always in the context of stalling after low carbing for a while. There was never evidence given, it was always hypothetical, a sort of rationalization. I don't believe that's what's happening. I believe it's just that we've reached the minimum homeostasis point we can reach by diet alone.

Here's an idea. For a man of 150lbs, 10% body fat is lean and that's 15lbs of body fat. Double the fat cells and we get 30lbs of body fat. To get back to 10% body fat just by releasing more fat from fat cells, we have to apply negative pressure in the form of semi-starvation, if we go by diet alone. How much, I don't know but I suspect it's quite a bit. Maybe in the range of 50-60% food intake. Now imagine we go from 150lbs ~ 10% body fat (15lbs fat) to 190lbs ~ 28% body fat (55lbs fat). How much food do we have to eat to go back to 10% body fat just by releasing more fat from fat cells now? At 190lbs ~ 28% body fat, we have around 3.5 times more fat cells than we used to.

I use the term body fat to designate fat and fat tissue combined. Growing fat cells takes time, years. So we won't grow 3.5 times more fat cells just by going from 150lbs/10% to 190lbs/28% in a few months. But if we've been 200lbs+ for 20 years, it's a safe bet we're going to stall with a significant amount of surplus body fat forever if we just go with diet alone.