What happens to those fat cells?


(Bunny) #41

Visceral adiposity is much different than subcutaneous fat cells; it only takes 48 hours of fasting to reduce the visceral fat around the internal organs by 25%? (…and inside the internal organs as well) That’s why Dr. Jason Fung is a genius!

That’s pretty dam fast compared to the subcutaneous fat cells willingness to give up the lipid droplets?

If we had any idea of how fast that is? It would be the equivalent of doing a ketogenic diet for 6 months at three meals per day to possibly reverse diabetes!


#42

Geez, put that way, I imagine it’s a great way to kick off LCHF/keto and speed the visceral fat change so as to access the subcutaneous more quickly? For those who have the lifestyle/schedule that allows them to fast, rest, and do all they need to do.


#43

So, the letting go of the watery fluid only means death of a fat cell after it’s reached its 10 year mark - or at a rate of 8% according to above posts.

Otherwise, fat cells just collapse and become skinny?


(Bunny) #44

That is what the ketogenic diet is for;

Maintenance :+1:


#45

Well, for those of us who can’t embark on 48 hour fasts though, it becomes the main, slow route for fat loss/recomposition before maintenance. I guess fasting is the fast lane!


(Complete legend) #46

Yes and no. I very VERY much doubt the “48 hours of fasting to reduce the visceral fat around the internal organs by 25%” idea.


(Karim Wassef) #47

Giving this idea more thought… that the useless lean mass in my legs was potentially empty fat cells made of protein vs. muscle cells…

I looked at my weightlifting logs after my refeed when I restarted my squats in earnest… muscle strength recovered very quickly to pre-fasting. While muscle density can vary… and hypertrophy and strength are not the same thing… I would say that the measurable loss of mass may not have been all muscle.


#48

I know the body tackles visceral fat first, but am unfamiliar with the fasting leveraging for initial visceral fat process. I wonder if Dr. Fung actually wrote or said that somewhere…


(Complete legend) #49

I don’t recall it, and I’ve read a fair bit of his stuff.


(Bunny) #50

Dr. Fung never said that:

I am stating this; Dr. Fung may not even be aware of it either, so what I am stating is independent of Dr. Jason Fung’s research.

This information comes from independent journals of endocrinology (peer reviewed), so that really compliments (cross-validates) Dr. Fung’s work.


(Bacon is the new bacon) #51

Think of it in evolutionary terms: fat cells are where the body stores its energy reserves. Deliberately down-sizing your “gas tank” could prove disastrous.

The adipose tissue serves both a short-term and a long-term purpose. In the short term, it is the holding tank or flywheel for energy, serving as short-term storage as energy comes into the body during digestion, and doling it back out at a steady rate between meals, especially during the overnight fast. It also serves as the reserve to fuel periods of fasting, so that after we finish eating one mammoth, the men have the energy to go out and hunt down another one. And of course, women need their more abundant body fat to fuel pregnancy and breast-feeding.


(Karim Wassef) #52

I’m not suggesting that the body jettison all the cells. However, if it’s going to remove lean mass (also not a good move evolutionary) with a plan to rebuild when resources are more plentiful, then the adipose cells should likewise be “rightsized”.

Let’s think of it this way… if you have a gas tank that was originally used to store a tanker truck’s reserve and you now drive a tiny Hyundai … why keep the massive gas tank… even if it’s empty? You’ve literally reduced your engine, wheels, frame, transmission, … everything else has been reduced… but the empty adiposites are spared?


#53

I’m guessing the body looks forward to the next feasting period while in a fast?

There’s also a lot of collagen tissue that supports the fat cells, I believe called the “extracellular matrix” that’s going to fluctuate. I’m not sure a DEXA would be able to detect this level of detail, but maybe an MRI would.


(Karim Wassef) #54

The articles I referenced also identify that adiposite apoptosis is part of the normal cycles. Just as with autophagy, we are in a constant state of recycling. Sometimes we interrupt it based on our dietary habits but it’s natural and heightened during fasting.


(Bacon is the new bacon) #55

Adipocytes do have a lifespan, but it’s something like eight or ten years or so. (Richard has posted about this.) There must be some mechanism for deciding whether to replace them or not, but the total number supposedly never declines. It is well-known, however, that muscle and bone have to be used to be retained, since they cary quite a metabolic cost.

It may be relevant to note that, if I have this correctly, the number of muscle cells doesn’t change, either, as the muscle grows and shrinks. Anyone know whether this is correct or not? It’s from something I read a long time ago.


(Karim Wassef) #56

I’ll keep digging into this MI-401 to see what the drivers are and if there are natural mechanisms (vs pharmaceuticals) that have the same effects.


(Bacon is the new bacon) #57

Where does this concern for reducing the number of fat cells come from? Are they harming anything, if they just hang around empty, or only partially filled?

Furthermore, wouldn’t reducing the number of adipocytes increase the level of insulin resistance? A number of serious researchers have hypothesized that the inability to increase the number of adipocytes is the determining factor that leads to insulin-resistance in most obese people. The metabolically healthy obese, under this hypothesis, would be those who are capable of making more fat cells to store the overload of fat. (I believe Dave Feldman has a series of graphics about this.) Another reason not to want to diminish one’s store of cells, it would seem.

Also, what happens to the glucose that is not turned into fat under the influence of MI-401?

And why the need for a drug in place of eating properly? Oh, sorry—pharmaceutical company profits. I forgot there, for a moment!

Thank heaven, all this becomes largely irrelevant on a well-formulated ketogenic diet.


(Karim Wassef) #58

It’s not concern. It’s a desire to understand the forces at work.

Not knowing how metabolism actually worked set me on a wasteful path for decades based on advice from experts & doctors.

Now, I personally want to understand autophagy and it’s rejuvenating effects - this is just one part of that.

Also, for obese people, the fat stores are massive - and on a ketogenic diet, the majority of these stores will never be re-used. So why maintain something that serves no purpose.

Maybe less adiposites means slower weight gain later in life? Maybe it means less efficiency so more energy is wasted as heat? Understanding how things work unlocks its own doors.

Oh - I share the pharma content only as a research source. I don’t believe there’s any need for that garbage.


(Bacon is the new bacon) #59

Ah, that makes sense. It just suddenly occurred to me that it might be a good idea to understand where you were coming from. After all, we know what happens when we assume . . . :rofl:

I’ve just been watching a video by Ivor Cummins, in which he reiterates the apparent connection between the ability to make more adipocytes and insulin sensitivity. I think it makes sense to have a capacity to store a lot of fat. I mean, think of a bear preparing for hibernation; in such a case it would make a lot of sense for as much energy as possible to be stored as fat, to be doled out over the winter. We don’t hibernate, of course, but I can see an advantage to still being able to put on weight as preparation for the winter, when game is scarcer.

I wouldn’t expect fewer adipocytes to prevent weight gain, since we know weight gain is a function of diet quality. It seems more logical to expect fewer adipocytes to have a greater problem handling an excess of fat, which would lead to visceral fat, ectopic fat, and intramuscular fat, all of which cause serious problems. Having enough fat cells to handle a load of fat would logically have to be a healthier situation overall.

Remember that it’s not the fat itself that’s the problem, it’s more fat than the body can handle that causes insulin resistance and all the consequent damage. Dr. Lustig quotes estimates that as many as 20% of obese people are perfectly healthy, metabolically speaking. They don’t develop heart disease, atherosclerosis, diabetes, gout, etc. Lustig also cites figures that 30% of lean people are metabolically deranged, but don’t realize that fact, because they are thin (on the outside, at least). In the view stated by Ivor and others, such TOFI’s are ill because they are incapable of creating more adipocytes, therefore they have become insulin-resistant even without becoming overweight. They’ve already run out of places to store fat healthily.


(Karim Wassef) #60

Totally agree… the question is still open “what happens to those fat cells?”

The literature is actually absurdly shallow on this topic. Even the authors start (as recently as 2017) stating that they don’t know.