Drastic diet 'reverses' Type 2 diabetes

[mcdonagh47]

Does anyone know how this trial has now been left at? are they going to continue with it? is it worth emailing DUK to find out? i wonder if it would work on say 800 cals or maybe 1000? i think i could possibly manage that but definately not 600

Hi carina,
the test just didn't involve cutting down to any old 600 calories. It was a highly calculated mix of essential nutrients in three liquid drinks a day plus salad leaves. Slurp three sachets of gunge a day and have a bit of rabbit food.
And as one medical comnmentator said, starvation has long been known to help with diabetes.

 

[Robster65]

As said before, I believe the aim was to prove the link between fatty deposits in/around the organs and diabetes (insulin resistance/impaired function).

If the symptoms didn't stay 'reversed', it would be presumably because the organs had clogged up again, thereby providing stronger evidence for the hypothesis.

For a widescale 'cure'/'reversal' to happen, they would need to find a way of clearing the fat deposits without such drastic measures. Someone may develop a pill to flush out the nasties, unless this is how current medication works.

Rob

 

[HelenM]

But the trial was in 2009 (?) - what was the position them six months after and a year after ? and now Its a temporary fix not a "reversal".

No idea if and when they will publish a follow up, this ones only just been published.

As said before, I believe the aim was to prove the link between fatty deposits in/around the organs and diabetes (insulin resistance/impaired function).
If the symptoms didn't stay 'reversed', it would be presumably because the organs had clogged up again, thereby providing stronger evidence for the hypothesis.

For a widescale 'cure'/'reversal' to happen, they would need to find a way of clearing the fat deposits without such drastic measures. Someone may develop a pill to flush out the nasties, unless this is how current medication works

.
I agree, but I also think it may have something to do with the reduction in circulating fatty acids. These are implicated in peripheral insulin resistance ie in the muscle cells as well as in the liver and pancreas.
The amount of insulin released when food is eaten isn't just dependent on the glucose level +amount of carb-protein.It also depends on the level of circulating fatty acids. If free fatty acids are high then more insulin will be released. They decrease when insulin is released with a meal. Metformin may have an effect on decreasing free fatty acids but even more so thiazolidinediones like Avandia and Actos... but they have been found to have other problems!
This is a very general article, and a bit old. There's loads of papers on insulin resistance and fatty acids but most are very very difficult to read without a specialist background. I can just about manage the intros and conclusions of many of them
http://www.medicinenet.com/script/main/art.asp?articlekey=52045

 

[Northerner]

Helen, I just wanted to thank you for all your input on this thread (and all the others too, of course!). I wouldn't know where to start looking for a lot of this stuff and I'm learning a lot 🙂

 

[timbla]

i too am really encouraged to note that this topic is still being discussed. i dont want to refer to specifics here, but i have seen on past occasions, posts about 'cures' and diets and remedies perhaps more holistic in nature, snuffed out with negative commentary before they have had a chance to develop. i concede that there must be a thin line dividing those in denial with those who are generally more optimistic about research which suggests a reversal of the big D is possible, perhaps i belong more to the former group, but still, all this talk about the 600 calorie diet suggests to me that there is a lot more optimism out there than i initially thought, and even if some are still discrediting it, i for one am buoyed by this, albeit tenuous link to hope that it reflects.

 

[Robster65]

Helen, I just wanted to thank you for all your input on this thread (and all the others too, of course!). I wouldn't know where to start looking for a lot of this stuff and I'm learning a lot 🙂

I agree. Thanks Helen for interpreting some of the technical details. 🙂

Some of the insulin/weight gain matters make sense now. All we need is a sure fire way of reducing circulating free fatty acids.

I presume lowering saturated fats would be a start. Plus an increase in exercise.

I feel sometimes that there is too much emphasis put on the carbs we eat, when the processing of those carbs is merely sympomatic of our sensitivity to insulin. If we could lower the resistance, ie. lower the free fatty acids, maybe low carbing wouldn't be so necessary ?

Just thinking out loud.🙂

Rob

 

[mcdonagh47]

to insulin. If we could lower the resistance, ie. lower the free fatty acids, maybe low carbing wouldn't be so necessary ?

Just thinking out loud.🙂

Rob

Insulin Resistance in Type 2s often has a physical basis. Insulin grabs a molecule of glucose and takes it to a cell. The insulin pops the glucose into a receptor base. The insulin then has to tether itself to the insulin receptor port and when it does that, signals go down to the nucleus of the cell and Glucose Transporters (GLUTs) swarm up to punch a hole in the cell wall and take the glucose into the cell. The insulin tethjered to the receptor port is either released to flaot off again or is taken apart and assimilated into the cell wall.
Powerful scanning microscopes have shown that in some T2s the insulin is malformed, lacking the tethers or just having stubby tethers, that it needs to tie itself to the cell and signal the cell that a delivery of glucose is waiting. With no signal being given, both the insulin and glucose just drift off.
So some IR in T2s is created by physically defective insulin - that's one reason injected insulin works well for most T2s - its always perfectly formed.

Other research into IR has looked at the GLUT transporters inside the cell and the signalling to them. One of them, GLUT4, has been suggested as a culprit that's not doing its job in some instances of IR.

The current research on the 600 calorie diet just looked at production of insulin in the Beta cells and didn't address IR at the level of the cells (presumably). That might help explain why the drastic diet didn't work for 40% of the participants.

The other issue with it is that T2s have no problem making insulin, they are awash with it, but it isnt being used. So why reduce the fat in the pancreas if IR will still cause major problems at the cell level ?

 

[Mark T]

...The current research on the 600 calorie diet just looked at production of insulin in the Beta cells and didn't address IR at the level of the cells (presumably). That might help explain why the drastic diet didn't work for 40% of the participants.

Interesting and a very informative post. I always assumed that this research was predominately concerned with insulin resistance - which was why I mostly discounted it. Certainly the test demographic was the 50+ obese insulin resistant type not the 30ish type like me (not saying that you can't have 50+ that are not insulin resistant or 30ish that are of course).

...The other issue with it is that T2s have no problem making insulin, they are awash with it, but it isnt being used. So why reduce the fat in the pancreas if IR will still cause major problems at the cell level ?

The research I've read seems to indicate that not all Type 2's have no problem making insulin. I'm certainly not convinced that I'm awash with insulin - certainly my urine c-peptide test seemed to indicate that I was lower then expected (but not a Type 1).

Many of the low carbers go for high unsaturated ketatonic fat diets and if my understanding is correct - this would lead to higher levels of free fatty acids circulating. If this is the case, shouldn't the low carbers have more insulin resistance? Or possibly it matters what type of fat is floating about.