Is the NHS 'soup and shake' type 2 diabetes diet really the solution we've been waiting for?

[everydayupsanddowns]

Do we have proof beta cells regenerate,

Yes. MRI scans, and path work. I think it’s the, functioning again with proper signalling rather than lost cells being replaced. I’m not sure if the ‘non responders’ had less recovery of beta cell function.

 

[childofthesea43]

And yet for me the weight loss wasnt enough to magically fix me as Taylor promises. I must maintain low carb to maintain bgl.

I seriously believe type 2 is at least two different classes of diabetes. One caused and solved almost entirely by weight and another that is far less weight dependent. Genetic in some way I guess or perhaps my beta cells are dead not dormant who knows? Not the research so far anyway.

Yes indeed, the weight-loss fix is not universal and Taylor acknowledged this from the start, although he thinks it works for most. Finding out why it does not always work is a research imperative. I guess you are probably right, that it’s something to do with the cells having become too exhausted by passage of time and hyperinsulinemia and perhaps a genetic factor as well.

 

[everydayupsanddowns]

1 - Does this diet work? And if so, will the improved BG levels be sustainable once the diet period is finished?

2 - Can you bear to do this diet?

For me, even if the answer to (1) is yes, on both counts, my answer to (2) is NOOOOOO!!!!!!!!!!!!!!!!!!!!!!

It seems an utterly unbearable diet to do. I couldn't do if for a day, let alone any longer, however good or effective it might be.

I seriously believe type 2 is at least two different classes of diabetes. One caused and solved almost entirely by weight and another that is far less weight dependent.

I think these are the two really key posts in this thread.

It is an option that works for some people.

It keeps working if those people maintain weight loss.

Personally I think it’s completely unfair to dismiss and rubbish the work either because it does not appeal to you as an individual, or because weight loss does not appear to have that effect in your case.

It should be available as an option to those who want to try it.

We need to be realistic that it is a) hard b) needs maintaining and c) is not a magic fixes-everything-for-everyone - but I simply don’t think it’s helpful to roast it as a concept whenever it is mentioned or enquired about.

 

[bulkbiker]

Agreed, it’s a formidable option and compliance may be poor. But it’s simple to prescribe and even if its results are very poor that will be a stupendous improvement over what the NHS has achieved for type-2s in the last few decades, which has been to lock hundreds of thousands of people into a one-way street of ever worsening medication and complications. So it’s the difference between bad and horrendous.

But what if there are other options that are neither extreme nor so liable to fail?

 

[bulkbiker]

Yes. MRI scans, and path work. I think it’s the, functioning again with proper signalling rather than lost cells being replaced. I’m not sure if the ‘non responders’ had less recovery of beta cell function.

Not really Mike, the MRI scans show ectopic fat and it's reduction I don't think they have ever been proven to show that cell function is impaired.. indeed as T2's overproduce insulin but insulin resistance means it doesn't work as it should, you could say that their pancreas is being overworked and not impaired at all.
This is precisely what Taylor et al miss.
They also usually fail to say that their patients were in ketosis (due to starvation and not design) but this could be an alternate explanation of why the method "works".
The ectopic fat is burned off as fuel and insulin resistance is corrected thereby restoring metabolic function to normal.
This could also be achieved by a far less harsh ketogenic diet which would be far easier to maintain.

 

[bulkbiker]

I have seen nothing in Taylor’s views that a long term crash diet is needed.

He recommends reducing food consumption by 33% post weight loss.
Sounds pretty drastic to me.

 

[everydayupsanddowns]

Not really Mike, the MRI scans show ectopic fat and it's reduction I don't think they have ever been proven to show that cell function is impaired.. indeed as T2's overproduce insulin but insulin resistance means it doesn't work as it should, you could say that their pancreas is being overworked and not impaired at all.
This is precisely what Taylor et al miss.
They also usually fail to say that their patients were in ketosis (due to starvation and not design) but this could be an alternate explanation of why the method "works".
The ectopic fat is burned off as fuel and insulin resistance is corrected thereby restoring metabolic function to normal.
This could also be achieved by a far less harsh ketogenic diet which would be far easier to maintain.

You have a different theory of the mechanism behind T2 than Taylor. So you view the work through that lens.

There are clinical compare-and-contrast studies that show low carb and keto diets are no more effective for diabetes management and weight loss than low calorie and that they are hard to maintain with high drop out rates.

But these don’t need to be shared here. Why?

Because low carb, and even keto DO work well for lots of members here, who find them effective and sustainable.

“T2D is characterized by insufficient secretion of insulin from the β-cells of the pancreatic islets, coupled with impaired insulin action in target tissues such as muscle, liver and fat (a condition termed insulin resistance).”

Q&A: insulin secretion and type 2 diabetes: why do β-cells fail?

www.ncbi.nlm.nih.gov

There‘s a bit of which-is-the-tail-and-which-is-the-dog in these models to my mind. I am happy to see them co-exist as a mix/blend of

Impaired insulin signalling
Impairment of organ function because of visceral fat
Loss of first phase insulin response
Insulin resistance (rusty keys and locks analogies)
Increased insulin production to overcome IR
Insufficient insulin availability because of IR

 

[bulkbiker]

T2D is characterized by insufficient secretion of insulin from the β-cells of the pancreatic islets,

That statement however is unproven and many would consider it nonsense.

It is precisely why we need to measure insulin production either directly or through c-peptide to see who is over and who is under producing and diagnose from that.

If the biggest diabetes charity in the UK could start advocating for that then how much could be saved by correctly diagnosing who has what.

 

[Robin]

He recommends reducing food consumption by 33% post weight loss.
Sounds pretty drastic to me.

It doesn’t sound drastic to me at all, bearing in mind that the people who needed to lose were probably eating larger portions than they needed before the weight loss, and the fact that a smaller body needs less fuel to maintain it. Add to that the fact that portion sizes are often ridiculously large when you eat out, I'm often outfaced by the amount of food on a plate in some restaurants, and even buying ready prepared sandwiches, sometimes OH and I share one between us. OK, we are small and elderly, not fit six footers doing a manual job, and some people may need that amount, but I think a lot of people don’t actually know what a 'normal' portion of food is.

 

[everydayupsanddowns]

I don't think they have ever been proven to show that cell function is impaired

You might find this interesting. Impaired beta cell function (and beta cell loss) has been part of the understanding of the progression of T2 since UKPDS. Previously thought to be an inevitable decline resulting in the need for exogenous insulin.

There are various studies into beta cell function recovery mentioned here, and also stuff from direct.

In parallel, the pancreatic triacylglycerol content decreased. In the more recent Diabetes Remission Clinical Trial (Direct), T2D remission and persistence of non-diabetic blood glucose control were achieved in 46% of patients on a low-calorie diet [37]. In a sub-study of 64 and 26 people from the intervention and control groups, respectively [43], the pancreatic fat content decreased whether glycemia normalized or not. Recovery of first-phase insulin release was seen in individuals with diabetes remission, which was durable at one year. Interestingly, subjects with sustained diabetes remission compared to those with relapse had less hepatic VLDL1-triglyceride production and VLDL1-palmitic acid content, no re-accumulation of pancreatic fat and maintained the first-phase insulin response by 2 years [44]. Persistence of remission was associated with improved pancreas morphology and declining pancreatic fat [45]. Sex does not seem to affect changes in intrapancreatic fat and VLDL1-triglyceride production after weight loss [46].

The Role of Beta Cell Recovery in Type 2 Diabetes Remission

Type 2 diabetes (T2D) has been considered a relentlessly worsening disease, due to the progressive deterioration of the pancreatic beta cell functional mass. Recent evidence indicates, however, that remission of T2D may occur in variable proportions of ...

www.ncbi.nlm.nih.gov

There’s a bunch of work that’s been undertaken about beta cell loss/dysfunction and impaired beta cell signalling in T2D, though a lot of it is a bit bamboozling for me.

 

[harbottle]

Why did travellor leave the forum?

Not really Mike, the MRI scans show ectopic fat and it's reduction I don't think they have ever been proven to show that cell function is impaired.. indeed as T2's overproduce insulin but insulin resistance means it doesn't work as it should, you could say that their pancreas is being overworked and not impaired at all.
This is precisely what Taylor et al miss.
They also usually fail to say that their patients were in ketosis (due to starvation and not design) but this could be an alternate explanation of why the method "works".
The ectopic fat is burned off as fuel and insulin resistance is corrected thereby restoring metabolic function to normal.
This could also be achieved by a far less harsh ketogenic diet which would be far easier to maintain.

No they didn't.
They showed pancreatic mass increased and insulin secretion returned to normal levels, both the first and second phase.
Type 2 diabetes is generally a problem of insulin secretion and lack of insulin.

The highest levels of insulin are seen in pre-diabetes, which is before the beta cells stop working.
The high levels are there because of constant release due to high blood sugar levels, not because there's a lot of insulin produced. Even if the secretion is blunted, there will be a lot of insulin because it's constantly being released as sugar is not coming back down for it to settle down into the 15 minute pulses that maintain the normal levels.

 

[bulkbiker]

Type 2 diabetes is generally a problem of insulin secretion and lack of insulin.

So please explain how insulin resistance develops?

The highest levels of insulin are seen in pre-diabetes, which is before the beta cells stop working.

Rarely if ever measured so I have no idea how you can make this as a statement of fact?

 

[bulkbiker]

The patient doesn’t have to understand, learn, know anything to take it up in that first phase.

I see that as a huge issue..
If people don't understand why they are doing something and what it is doing to them then how on earth can they benefit from it long term?
It's another case of subcontracting your health to a HCP rather than educating people on how to address the root cause of the problem.

 

[Chris Hobson]

My update as promised. I have been to see my specialist nurse. She said that I was correct to stop taking the linagliptin when the hypos occurred. I am now off the meds for four months after which I will have another blood test to see how that is working. I have put a slight amount of weight back on, I'm still under 75 kilos, just. I have been too busy to go swimming. For the last couple of months or so. My plan is to get back to swimming and cycling to see if I can get down to 70 kilos again and see how it works out.

 

[Dragonheart]

There are clinical compare-and-contrast studies that show low carb and keto diets are no more effective for diabetes management and weight loss than low calorie and that they are hard to maintain with high drop out rates.

Pretty much the same for low calorie diets then as they seem to fail a lot of people too? Some methods will suit some types of people. The fundamental key is knowing about both/all so if one approach fails you then you have to know about the alternatives.

There‘s a bit of which-is-the-tail-and-which-is-the-dog in these models to my mind. I am happy to see them co-exist as a mix/blend of

Impaired insulin signalling
Impairment of organ function because of visceral fat
Loss of first phase insulin response
Insulin resistance (rusty keys and locks analogies)
Increased insulin production to overcome IR
Insufficient insulin availability because of IR

Going back to my point about type 2 being a catch all for various types of diabetes and trying to treat us a homogenous group will always fail some parts of it

 

[AndBreathe]

Taylor’s team has proved that the beta cells, relieved of the burden of excess internal fat, will for most people recover normal secretion levels and normal dynamics in the first-phase response.

Could you point me to that please? I find Taylor often hypothesises on "stuff", so would like to see what he measures, when and how. (I'm like that.)

Thanks

 

[AndBreathe]

In my own case - and I would not generalise to all by any means - I simply lost weight and it all got better. So for me it was as helpful as anything could be, other than a miracle of rejuvenation.

My point is, some of those with T2 aren't overweight, and some of those diagnosed T2 aren't actually even T2. The could be LADA, Mody or T3c, just off the top of my head.

In my experience, these days, medics prescribe weight loss for everything. I even had a telephone consultation with a rheumatologist, relating to some arthritic joints in my hands. She suggested my condition would improve by posing weight. I'm afraid the tone of my query of how many of my 48kg I should lose might not have been too positive.

 

[nonethewiser]

It doesn’t sound drastic to me at all, bearing in mind that the people who needed to lose were probably eating larger portions than they needed before the weight loss, and the fact that a smaller body needs less fuel to maintain it. Add to that the fact that portion sizes are often ridiculously large when you eat out, I'm often outfaced by the amount of food on a plate in some restaurants, and even buying ready prepared sandwiches, sometimes OH and I share one between us. OK, we are small and elderly, not fit six footers doing a manual job, and some people may need that amount, but I think a lot of people don’t actually know what a 'normal' portion of food is.

Great Post @Robin & couldn't agree more.

 

[childofthesea43]

I see that as a huge issue..
If people don't understand why they are doing something and what it is doing to them then how on earth can they benefit from it long term?
It's another case of subcontracting your health to a HCP rather than educating people on how to address the root cause of the problem.

I agree absolutely.

Could you point me to that please? I find Taylor often hypothesises on "stuff", so would like to see what he measures, when and how. (I'm like that.)

Thanks

Try this paper:

https://eprints.ncl.ac.uk/file_store/production/270387/FC3A415E-228D-477C-8007-438870274DDA.pdf

 

[childofthesea43]

My point is, some of those with T2 aren't overweight, and some of those diagnosed T2 aren't actually even T2. The could be LADA, Mody or T3c, just off the top of my head.

In my experience, these days, medics prescribe weight loss for everything. I even had a telephone consultation with a rheumatologist, relating to some arthritic joints in my hands. She suggested my condition would improve by posing weight. I'm afraid the tone of my query of how many of my 48kg I should lose might not have been too positive.

Indeed, at 48kg there can be nothing left to lose fat-wise. What was the figure X on diagnosis? If X>48 how long did it take to reduce to 48? If there was such a reduction how soon was it initiated after diagnosis?