Personal Fat Threshold...thoughts

[mhtyler]

I think one of the two most brilliant syntheses that Prof. Taylor has come up with is the concept of the Personal Fat Threshold. In starts with a definition of diabetes 2 as a disease of too much fat in the body, but specifically, it means too much ectopic fat since subcutaneous fat is healthy or at least metabolically neutral. What is so brilliant about it is that it accounts for why a percentage of people can be obese without diabetes 2 (T2D) and slim people can have it as well. Some people can't produce very much subcutaneous fat, and at the other extreme, some can produce huge amounts. I remember seeing a poster in my doctor's office saying that for every pound of fat you see on the outside, there is a pound inside. I don't know if that's even generally true, but Prof. Taylor did try and destroy his own hypothesis in a study that ended up confirming it. Two studies later, and it is still holding up. Not everyone in the medical profession is buying into this though, and in fact, until recent years remission of T2D was considered impossible. Now its largely accepted on both sides of the pond as at least being possible in a percentage; mostly people who catch it early. At the end of Prof. Taylor's Counterbalance study, he acknowledges that although his responders (43%) achieved and maintained remission for 6 months there is a very real question of how long it can be maintained. He considers that it's likely to be maintained for as long as weight loss is maintained, but he also acknowledges the difficulty of doing that. What isn't clear ...to me at least... is the mechanism of the Personal Fat Threshold at the cellular level. Not that as a layman I'm likely to fully understand it.

 

[harbottle]

It may be the weight loss removing the lipotoxicity that is known to cause problems with beta cells (Along with glucotoxicity) although it's never been shown that they can recover from it (They can from glucotoxicity)

People who are overweight tend to release more FFAs into the bloodstream, and there may be some genetic factors at play.

 

[mhtyler]

It may be the weight loss removing the lipotoxicity that is known to cause problems with beta cells (Along with glucotoxicity) although it's never been shown that they can recover from it (They can from glucotoxicity)

People who are overweight tend to release more FFAs into the bloodstream, and there may be some genetic factors at play.

That's an interesting distinction between toxicity from fat vs glucose. Either way it strikes me both will go down with loss of weight. In Prof. Taylor's studies it's clearly shown that some can recover pancreas function, and others cannot. Time seems to be the key factor, since early weight loss after diagnosis almost guarantees remission in anyone, whereas more than 10 years after diagnosis there's a likelihood that you will not. That said, some can recover pancreas function at 25 years on...they are outliers though. It would seem that genetics plays a part in the latter. He also makes a distinction between beta cell loss, and dedifferentiation. That's one of the big deals I read about in research these days. It's a distinction lost on me as a layman though, since broken is broken.

 

[PerSpinasAdAstra]

I don't know what to think about the Personal Fat Threshold hypothesis. There is definitely evidence that genetics plays a role in where the body stores fat, such as the increased prevalence of visceral adipose fat (and T2 diabetes) at lower BMI in the Indian population. What I don't understand is why a person might be genetically disposed to ectopic fat storage above a specific weight threshold. Maybe it really is the case that adipose tissue becomes 'full' at a certain point and fat has nowhere to go other than ectopic storage. If that's the case though, what happens when there is no more ectopic capacity? If someone passes their personal fat threshold, stores a load of fat ectopically and in visceral adipose tissue, and then continues to put on weight, does it suddenly go back to being stored in subcutaneous adipose tissue? It's not as if there is any known limit to how fat a person can get.

This paper lays out an alternative theory. It suggests that it's not about a fat storage threshold but about the rate of energy consumption. The idea is that when fat cells grow too large too fast they become inflamed, insulin resistant and they 'leak' free fatty acids (FFA) into the blood. If this happens at a large enough scale then FFA levels in the blood rise and this leads to fat uptake by organ tissue which is stored ectopically. If this theory is correct then over-eating causes fat accumulation in the liver and pancreas, not passing a particular fat storage threshold. This theory accounts for why a person can be obese and not have a fatty liver or be especially insulin resistant - if weight is put on gradually, little by little, then you don't get the 'too large too fast' problem in fat cells to the same extent, thus no big rise in FFA levels, thus little or no ectopic fat storage.

The role of fatty acids in insulin resistance

Insulin resistance is a multi-faceted disruption of the communication between insulin and the interior of a target cell. The underlying cause of insulin resistance appears to be inflammation that can either be increased or decreased by the fatty acid ...

www.ncbi.nlm.nih.gov

I don't know what to think so I'm hedging my bets. I'll lose a load of weight and then avoid eating too much in a single sitting. No more large meals - if I get a big portion at a restaurant for example I'll leave some on the plate. That will be a useful practise anyway to help maintain my weight, and it means that whether Roy Taylor or the authors of this paper are correct I should still be able to avoid fat accumulation in my liver and pancreas. Perhaps neither theory is correct, but there's not much I can do about that so I'll stick to be best plan I can come up with.

 

[trophywench]

I dunno in the medical sense. I do know that we have one severely autistic great grandchild and he gets very upset and completely refuses to eat certain foods at all hence must not be allowed to spot eg mashed spud which he's super fond of eating anywhere other than the portion on his plate else he'll automatically move himself to the other person, mainly adults, instantly climb on their lap but absolutely not should you have poisoned yours with eg gravy or by allowing it to touch another type of food, shudder, and with his beatific smile expect to have his desire fulfilled by that person. 'No - you need to eat more of your dinner before I share mine with you.' is a complete and utter waste of breath telling him. He is wired to have to eat every single morsel of whatever it is, before anything else on the plate. You could grow old and die if it's a spoonful of sweetcorn. Every single kernel, one at a time, and mega extremely chewed before swallowing.

I'm not autistic at all - BUT if you put to much of anything at all on my plate, I'm overfaced and can't enjoy eating practically anything on there. Husband's a bugger for this - That's not enough whatever proclaims he and proceeds to transfer some of what's on his plate to mine. We've only been having this conversation practically every day since 1998 - so why the hell am I still having to keep telling him. Aargh! We're both averse to food waste, hence why I only put myself what I know I'll eat.

But, I agree on planning to leave some of whatever on that plate can be a good place to start before you risk getting too strict with yourself - and I have sometimes got to that stage - so there is rather a narrow line between the two.

We each just have to find our very own balance and there's no exactly right way guaranteed to suit everyone.

 

[mhtyler]

I don't know what to think about the Personal Fat Threshold hypothesis. There is definitely evidence that genetics plays a role in where the body stores fat, such as the increased prevalence of visceral adipose fat (and T2 diabetes) at lower BMI in the Indian population. What I don't understand is why a person might be genetically disposed to ectopic fat storage above a specific weight threshold.

I don't think it's a weight threshold that Prof. Taylor is talking about, It's a subcutaneous fat threshold. That is why he points out that you can clear the fat from your liver and pancreas with 15 kg of weight loss regardless of whether you remain obese or not.

 

[PerSpinasAdAstra]

I don't think it's a weight threshold that Prof. Taylor is talking about, It's a subcutaneous fat threshold. That is why he points out that you can clear the fat from your liver and pancreas with 15 kg of weight loss regardless of whether you remain obese or not.

My interpretation of his work is that he's proved a person can burn off fat in and around the liver and pancreas with weight loss, and that 15Kg of loss is enough to achieve this for most overweight people. He's further proved that putting weight (fat) back on can lead to fat building up in and around these organs again. He claims to have proved the personal fat threshold hypothesis by doing this. However, he hasn't actually proved that it's the amount of re-gained fat that led to the problem recurring rather than the rate at which that weight was regained. This is why I'm a little uncertain. I don't question the results of the weight loss and the value of his work but I'm not so convinced about the personal threshold idea that I'm willing to dismiss the other possibility.